| characterization of the activity and expression of arginine decarboxylase in human and animal chlamydia pathogens. | chlamydia pneumoniae encodes a functional arginine decarboxylase (argdc), aaxb, that activates upon self-cleavage and converts l-arginine to agmatine. in contrast, most chlamydia trachomatis serovars carry a missense or nonsense mutation in aaxb abrogating activity. the g115r missense mutation was not predicted to impact aaxb functionality, making it unclear whether aaxb variations in other chlamydia species also result in enzyme inactivation. to address the impact of gene polymorphism on functi ... | 2012 | 23043454 |
| the cationic liposomal adjuvants caf01 and caf09 formulated with the major outer membrane protein elicit robust protection in mice against a chlamydia muridarum respiratory challenge. | two cationic liposomal adjuvants caf01 and caf09 were formulated with the native or the recombinant chlamydia muridarum major outer membrane protein (nmomp and rmomp). balb/c mice were immunized with the four vaccine formulations using the subcutaneous followed by the intranasal (i.n.) routes. as positive controls mice were inoculated i.n. with live c. muridarum and negative controls received i.n. minimal essential medium (mem). four weeks after the last immunization mice were challenged i.n. wi ... | 2017 | 28238632 |
| [role of light signal pathway in chlamydia muridarum urogenital infection in mice]. | to study the role of lymphotoxin-like inducible protein that competes with glycoprotein d for herpesvirus entry on t cells (light) in the development of protective immunity and pathology during chlamydia muridarum urogenital infection in mice. | 2015 | 26211324 |
| in vivo and ex vivo imaging reveals a long-lasting chlamydial infection in the mouse gastrointestinal tract following genital tract inoculation. | intravaginal infection with chlamydia muridarum in mice can ascend to the upper genital tract, resulting in hydrosalpinx, a pathological hallmark for tubal infertility in women infected with c. trachomatis. here, we utilized in vivo imaging of c. muridarum infection in mice following an intravaginal inoculation and confirmed the rapid ascent of the chlamydial organisms from the lower to upper genital tracts. unexpectedly, the c. muridarum-derived signal was still detectable in the abdominal area ... | 2015 | 26099591 |
| update on chlamydia trachomatis vaccinology. | attempts to produce a vaccine to protect against chlamydia trachomatis-induced trachoma were initiated more than 100 years ago and continued for several decades. using whole organisms, protective responses were obtained. however, upon exposure to c. trachomatis, disease exacerbation developed in some immunized individuals, precluding the implementation of the vaccine. evidence of the role of c. trachomatis as a sexually transmitted pathogen started to emerge in the 1960s, and it soon became evid ... | 2017 | 28228394 |
| comparison of murine cervicovaginal infection by chlamydial strains: identification of extrusions shed in vivo. | chlamydia trachomatis is the leading cause of bacterial sexually transmitted infections (stis) and preventable blindness. untreated, asymptomatic infection as well as frequent re-infection are common and may drive pelvic inflammatory disease, ectopic pregnancy, and infertility. in vivo models of chlamydial infection continue to be instrumental in progress toward a vaccine and further elucidating the pathogenesis of this intracellular bacterium, however significant gaps in our understanding remai ... | 2017 | 28217555 |
| cd103+ lung dendritic cells (ldcs) induce stronger th1/th17 immunity to a bacterial lung infection than cd11b(hi) ldcs. | recent studies suggest differential roles for cd103+ and cd11b(hi) lung dendritic cells (ldcs) in host defense against viral and bacterial infections. in this study, we examined the contribution of these ldc subsets in protective immunity to chlamydial lung infection using a chlamydia muridarum mouse infection model. we found that cd103+ ldcs showed higher expression of costimulatory molecules (cd40, cd80 and cd86) and increased production of cytokines (il-12p70, il-10, il-23 and il-6) compared ... | 2017 | 28194020 |
| micrornas modulate pathogenesis resulting from chlamydial infection in mice. | not all women infected with chlamydiae develop upper genital tract disease, but the reason(s) for this remains undefined. host genetics and hormonal changes associated with the menstrual cycle are possible explanations for variable infection outcomes. it is also possible that disease severity depends on the virulence of the chlamydial inoculum. it is likely that the inoculum contains multiple genetic variants, differing in virulence. if the virulent variants dominate, then the individual is more ... | 2017 | 27799333 |
| ccl19-ccr7-dependent reverse transendothelial migration of myeloid cells clears chlamydia muridarum from the arterial intima. | regions of the normal arterial intima predisposed to atherosclerosis are sites of ongoing monocyte trafficking and also contain resident myeloid cells with features of dendritic cells. however, the pathophysiological roles of these cells are poorly understood. here we found that intimal myeloid cells underwent reverse transendothelial migration (rtm) into the arterial circulation after systemic stimulation of pattern-recognition receptors (prrs). this process was dependent on expression of the c ... | 2016 | 27668800 |
| chlamydial plasmid-dependent pathogenicity. | most chlamydia species carry a 7.5kb plasmid encoding eight open reading frames conventionally called plasmid glycoproteins 1-8 or pgp1-8. although the plasmid is not critical for chlamydial growth in vitro, its role in chlamydial pathogenesis is clearly demonstrated in the genital tracts of mice infected with chlamydia muridarum, a model for investigating the human pathogen chlamydia trachomatis. plasmid-free c. trachomatis is also attenuated in both the mouse genital tract and nonhuman primate ... | 2017 | 27712952 |
| antigen specific immune response in chlamydia muridarum genital infection is dependent on murine micrornas-155 and -182. | anti-chlamydial immunity involves efficient presentation of antigens (ag) to effector cells resulting in ag-specific immune responses. there is limited information on inherent underlying mechanisms regulating these events. previous studies from our laboratory have established that select micrornas (mirs) function as molecular regulators of immunity in chlamydia muridarum (cm) genital infection. in this report, we investigated immune cell type-specific mirs, i.e. mir-155 and -182, and the role in ... | 2016 | 27556515 |
| host nectin-1 promotes chlamydial infection in the female mouse genital tract, but is not required for infection in a novel male murine rectal infection model. | chlamydia trachomatis is the most common bacterial sexually transmitted pathogen, but more than 70% of patients fail to seek treatment due to the asymptomatic nature of these infections. women suffer from numerous complications from chronic chlamydial infections, which include pelvic inflammatory disease and infertility. we previously demonstrated in culture that host cell nectin-1 knockdown significantly reduced chlamydial titers and inclusion size. here, we sought to determine whether nectin-1 ... | 2016 | 27486990 |
| mri as a novel in vivo approach for assessing structural changes of chlamydia pathology in a mouse model. | chlamydia trachomatis is among the most prevalent of sexually transmitted diseases. while chlamydia infection is a reportable event and screening has increased over time, enhanced surveillance has not resulted in a reduction in the rate of infections, and chlamydia infections frequently recur. the development of a preventative vaccine for chlamydia may be the only effective approach for reducing infection and the frequency of pathological outcomes. current vaccine research efforts involve time c ... | 2016 | 27467585 |
| chlamydial antibiotic resistance and treatment failure in veterinary and human medicine. | the chlamydiaceae are widespread pathogens of both humans and animals. chlamydia trachomatis infection causes blinding trachoma and reproductive complications in humans. chlamydia pneumoniae causes human respiratory tract infections and atypical pneumonia. chlamydia suis infection is associated with conjunctivitis, diarrhea, and failure to gain weight in domestic swine. chlamydial infections in humans and domesticated animals are generally controlled by antibiotic treatment-particularly macrolid ... | 2017 | 27218014 |
| the chlamydia muridarum organisms fail to auto-inoculate the mouse genital tract after colonization in the gastrointestinal tract for 70 days. | chlamydia muridarum is known to colonize in the gastrointestinal tract for long periods of time, which has been hypothesized to serve as a reservoir for spreading to the genital tract. to test this hypothesis, a luciferase-expressing c. muridarum was used to establish a long-lasting infection in the mouse gastrointestinal tract following either intragastric or intrarectal inoculations. in vivo imaging revealed significant bioluminescent signals mainly in the mouse abdominal area throughout the e ... | 2016 | 27192556 |
| biophysical principles predict fitness landscapes of drug resistance. | fitness landscapes of drug resistance constitute powerful tools to elucidate mutational pathways of antibiotic escape. here, we developed a predictive biophysics-based fitness landscape of trimethoprim (tmp) resistance for escherichia coli dihydrofolate reductase (dhfr). we investigated the activity, binding, folding stability, and intracellular abundance for a complete set of combinatorial dhfr mutants made out of three key resistance mutations and extended this analysis to dhfr originated from ... | 2016 | 26929328 |
| involvement of lysosome membrane permeabilization and reactive oxygen species production in the necrosis induced by chlamydia muridarum infection in l929 cells. | chlamydiae, obligate intracellular bacteria, are associated with a variety of human diseases. the chlamydial life cycle undergoes a biphasic development: replicative reticulate bodies (rbs) phase and infectious elementary bodies (ebs) phase. at the end of the chlamydial intracellular life cycle, ebs have to be released to the surrounded cells. therefore, the interactions between chlamydiae and cell death pathways could greatly influence the outcomes of chlamydia infection. however, the underlyin ... | 2016 | 26838343 |
| iga modulates respiratory dysfunction as a sequela to pulmonary chlamydial infection as neonates. | neonatal chlamydia lung infections are associated with serious sequelae such as asthma and airway hyper-reactivity in children and adults. our previous studies demonstrated the importance of th-1 type cytokines, il-12 and ifn-γ in protection against neonatal pulmonary chlamydial challenge; however, the role of the humoral arm of defense has not been elucidated. we hypothesized that b-cells and iga, the major mucosal antibody, play a protective role in newborns against development of later life r ... | 2016 | 26755533 |
| the chromosome-encoded hypothetical protein tc0668 is an upper genital tract pathogenicity factor of chlamydia muridarum. | we previously associated a missense mutation of the tc0668 gene of serial in vitro-passaged chlamydia muridarum, a murine model of human urogenital c. trachomatis, with severely attenuated disease development in the upper genital tract of female mice. since these mutants also contained a tc0237 q117e missense mutation that enhances their in vitro infectivity, an effort was made here to isolate and characterize a tc0668 single mutant to determine its individual contribution to urogenital pathogen ... | 2015 | 26597987 |
| modeling the transcriptome of genital tract epithelial cells and macrophages in healthy mucosa versus mucosa inflamed by chlamydia muridarum infection. | chlamydia trachomatis urogenital serovars are intracellular bacteria that parasitize human reproductive tract epithelium. as the principal cell type supporting bacterial replication, epithelial cells are central to chlamydia immunobiology initially as sentries and innate defenders, and subsequently as collaborators in adaptive immunity-mediated bacterial clearance. in asymptomatic individuals who do not seek medical care a decisive struggle between c. trachomatis and host defenses occurs at the ... | 2015 | 26519447 |
| a vaccine formulated with the major outer membrane protein can protect c3h/hen, a highly susceptible strain of mice, from a chlamydia muridarum genital challenge. | c3h/hen female mice were vaccinated with native chlamydia muridarum major outer membrane protein (momp), using montanide+cpg or alum+cpg as adjuvants. negative control groups were immunized with ovalbumin (ova) and the same adjuvants. as positive control, mice were inoculated intranasally with live chlamydia. mice were challenged in the ovarian bursa with 10(5) c. muridarum inclusion forming units. six weeks after the genital challenge the animals were caged with male mice and monitored for preg ... | 2015 | 26423798 |
| pulmonary chlamydia muridarum challenge activates lung interstitial macrophages which correlate with ifn-γ production and infection control in mice. | protective immunity to the pathogen chlamydia is dependent on a robust ifn-γ response generated by innate and adaptive lymphocytes. here we assess the role of the macrophage in orchestrating a protective response in vivo to the murine pathogen, chlamydia muridarum. during acute pulmonary and peritoneal infection, resident macrophages in both sites are infected with c. muridarum and adopt an inflammatory phenotype. in the lung, this activation is restricted to interstitial macrophages, which harb ... | 2015 | 26344246 |
| role of stat1 in chlamydia-induced type-1 interferon production in oviduct epithelial cells. | we previously reported that chlamydia muridarum-infected murine oviduct epithelial cells (oe cells) secrete interferon β (ifn-β) in a mostly tlr3-dependent manner. however, c. muridarum-infected tlr3-deficient oe cells were still able to secrete detectable levels of ifn-β into the supernatants, suggesting that other signaling pathways contribute to chlamydia-induced ifn-β synthesis in these cells. we investigated the role of stat1 as a possible contributor in the chlamydia-induced type-1 ifn pro ... | 2015 | 26262558 |
| nk cells modulate the lung dendritic cell-mediated th1/th17 immunity during intracellular bacterial infection. | the impact of the interaction between nk cells and lung dendritic cells (ldcs) on the outcome of respiratory infections is poorly understood. in this study, we investigated the effect and mechanism of nk cells on the function of ldcs during intracellular bacterial lung infection of chlamydia muridarum in mice. we found that the naive mice receiving ldcs from c. muridarum-infected nk-cell-depleted mice (nk-ldcs) showed more serious body weight loss, bacterial burden, and pathology upon chlamydial ... | 2015 | 26222048 |
| detection of chlamydia infection in peromyscus species rodents from sylvatic and laboratory sources. | to determine if chlamydia muridarum, or other chlamydiae, are enzootic in rodents, we probed a serum bank of wild peromyscus spp. mice for immunoglobulin g-antibody reactivity to ultraviolet light-inactivated c. muridarum elementary bodies (ebs) using an enzyme-linked immunoassay. applying a cut-off for a positive reaction of od(405) nm = 0.1 at a 1:20 dilution, we found titratable antibody reactivity in 190 of 247 specimens surveyed (77%, mean od(405) = 0.33 ± 0.26, range = 0.11-1.81, median = ... | 2016 | 26733499 |
| computational modeling of tc0583 as a putative component of the chlamydia muridarum v-type atp synthase complex and assessment of its protective capabilities as a vaccine antigen. | numerous chlamydia trachomatis proteins have been identified as potential subunit vaccines, of which the major outer-membrane protein (momp) has, so far, proven the most efficacious. recently, subunit a of the v-type atp synthase (atpase; tc0582) complex was shown to elicit partial protection against infection. computational modeling of a neighboring gene revealed a novel subunit of the v-type atpase (tc0583). to determine if this newly identified subunit could induce protection and/or enhance t ... | 2016 | 26706820 |
| quantitative in vivo detection of chlamydia muridarum associated inflammation in a mouse model using optical imaging. | chlamydia trachomatis is a bacterial sexually transmitted disease with over 1.3 million cases reported to the cdc in 2010. while chlamydia infection is easily treated with antibiotics, up to 70% of infections are asymptomatic and go untreated. the current mouse model relies on invasive upper genital tract gross pathology readouts at ~60-80 days postinfection. high throughput optical imaging through the use of biomarkers has been successfully used to quickly evaluate several disease processes. he ... | 2015 | 26663988 |
| the p47phox deficiency significantly attenuates the pathogenicity of chlamydia muridarum in the mouse oviduct but not uterine tissues. | the chlamydia muridarum induction of the upper genital tract pathology in mice has been used to investigate the mechanisms of chlamydial pathogenesis. we report that the ncf1 (neutrophil cytosolic factor1)-encoded p47phox (phagocyte oxidase), an essential subunit of nicotinamide adenine dinucleotide phosphate (nadph)-oxidase, contributes significantly to c. muridarum induction of hydrosalpinx. mice lacking p47phox (p47phox-deficient) were no longer able to develop significant hydrosalpinx follow ... | 2016 | 26645958 |
| intrauterine infection with plasmid-free chlamydia muridarum reveals a critical role of the plasmid in chlamydial ascension and establishes a model for evaluating plasmid-independent pathogenicity. | intravaginal infection with plasmid-competent but not plasmid-free chlamydia muridarum induces hydrosalpinx in mouse upper genital tract, indicating a critical role of the plasmid in chlamydial pathogenicity. to evaluate the contribution of the plasmid to chlamydial ascension and activation of tubal inflammation, we delivered plasmid-free c. muridarum directly into the endometrium by intrauterine inoculation. we found that three of the six mouse strains tested, including cba/j, c3h/hej, and c57b ... | 2015 | 25870225 |
| murine microrna-214 regulates intracellular adhesion molecule (icam1) gene expression in genital chlamydia muridarum infection. | the hallmark of chlamydial infection is the development of upper genital pathology in the form of hydrosalpinx and oviduct and/or tubal dilatation. although molecular events leading to genital tissue presentation and cellular architectural remodelling are unclear, early-stage host immune responses are believed to contribute to these long-term sequelae. recently, we reported the contribution of selected infection-associated micrornas (mirs) in the generation of host immunity at early-stage infect ... | 2015 | 25865776 |
| chlamydia muridarum induction of glandular duct dilation in mice. | although chlamydia-induced hydrosalpinx in women and mice has been used as a surrogate marker for tubal infertility, the medical relevance of nontubal pathologies, such as uterine horn dilation, developed in mice following chlamydial infection remains unclear. we now report that the uterine horn dilation correlates with glandular duct dilation detected microscopically following chlamydia muridarum infection. the dilated glandular ducts pushed the uterine horn lumen to closure or dilation and eve ... | 2015 | 25824829 |
| outer membrane proteins preferentially load mhc class ii peptides: implications for a chlamydia trachomatis t cell vaccine. | cd4 t cell immune responses such as interferon-γ and tumor necrosis factor-α secretion are necessary for chlamydia immunity. we used an immunoproteomic approach in which chlamydia trachomatis and chlamydia muridarum-derived peptides presented by mhc class ii molecules on the surface of infected dendritic cells (dcs) were identified by tandem mass spectrometry using bone marrow derived dcs (bmdcs) from mice of different mhc background. we first compared the c. muridarum immunoproteome in c3h mice ... | 2015 | 25738816 |
| in vitro passage selects for chlamydia muridarum with enhanced infectivity in cultured cells but attenuated pathogenicity in mouse upper genital tract. | although modern chlamydia muridarum has been passaged for decades, there are no reports on the consequences of serial passage with strong selection pressure on its fitness. in order to explore the potential for pasteurian selection to induce genomic and phenotypic perturbations to c. muridarum, a starter population was passaged in cultured cells for 28 generations without standard infection assistance. the resultant population, designated cmg28, displays markedly reduced in vitro dependence on c ... | 2015 | 25712926 |
| genomic variant representation in a chlamydia population is dynamic and adaptive with dependence on in vitro and in vivo passage. | we have previously shown that chlamydia muridarum has multiple genomic variants that concomitantly vary in their in vitro and in vivo phenotype. herein, we used real-time polymerase chain reaction-based genotyping assays to query plaque-cloned isolates of c. muridarum for the frequency of eight selected polymorphisms. these strains had no history of passage in vivo since their original isolation from laboratory mice. there was significant variance in the frequency of two of the eight polymorphis ... | 2015 | 25673672 |
| chlamydial lung infection induces transient il-9 production which is redundant for host defense against primary infection. | il-9/th9 responses are recently found to be important for innate and adaptive immunity particularly in parasitic infections. to date, the study on the role of il-9 in bacterial infections is limited and the reported data are contradictory. one reported function of il-9/th9 is to modulate th1/th17 responses. since our and others' previous work has shown a critical role of th1 and th17 cells in host defense against chlamydial lung infection, we here examined the role of il-9 responses in chlamydia ... | 2015 | 25646821 |
| high chlamydia burden promotes tumor necrosis factor-dependent reactive arthritis in skg mice. | chlamydia trachomatis is a sexually transmitted obligate intracellular pathogen that causes inflammatory reactive arthritis, spondylitis, psoriasiform dermatitis, and conjunctivitis in some individuals after genital infection. the immunologic basis for this inflammatory response in susceptible hosts is poorly understood. as zap-70(w163c) -mutant balb/c (skg) mice are susceptible to spondylo-arthritis after systemic exposure to microbial β-glucan, we undertook the present study to compare respons ... | 2015 | 25624153 |
| tumor necrosis factor (tnf) receptor superfamily member 1b on cd8+ t cells and tnf receptor superfamily member 1a on non-cd8+ t cells contribute significantly to upper genital tract pathology following chlamydial infection. | we demonstrated previously that tumor necrosis factor α (tnf-α)-producing chlamydia-specific cd8(+) t cells cause oviduct pathological sequelae. | 2015 | 25552370 |
| identification of plasmid-free chlamydia muridarum organisms using a pgp3 detection-based immunofluorescence assay. | chlamydia possesses a conserved 7.5 kb plasmid that is known to play an important role in chlamydial pathogenesis, since some chlamydial organisms lacking the plasmid are attenuated. the chlamydial transformation system developed recently required the use of plasmid-free organisms. thus, the generation and identification of plasmid-free organisms represent a key step in understanding chlamydial pathogenic mechanisms. a tricolor immunofluorescence assay for simultaneously detecting the plasmid-en ... | 2015 | 26059520 |
| chlamydia muridarum infection of macrophages elicits bactericidal nitric oxide production via reactive oxygen species and cathepsin b. | the ability of certain species of chlamydia to inhibit the biogenesis of phagolysosomes permits their survival and replication within macrophages. the survival of macrophage-adapted chlamydiae correlates with the multiplicity of infection (moi), and optimal chlamydial growth occurs in macrophages infected at an moi of ≤1. in this study, we examined the replicative capacity of chlamydia muridarum in the raw 264.7 murine macrophage cell line at different mois. c. muridarum productively infected th ... | 2015 | 26015483 |
| plasmid-encoded pgp5 is a significant contributor to chlamydia muridarum induction of hydrosalpinx. | we have previously shown that the plasmid-encoded pgp3 is a major virulence factor for c. muridarum induction of hydrosalpinx. we now report that pgp5 also plays a significant role in the development of hydrosalpinx following c. muridarum induction. pgp5 deficiency was introduced via either in-frame deletion (cm-δpgp5) or premature stop codon installation (cm-pgp5s). mice infected with either cm-δpgp5 or cm-pgp5s developed hydrosalpinges at significantly reduced levels with an incidence rate of ... | 2015 | 25915629 |
| [th17 lymphocytes in bacterial infections]. | th17 cells are a relatively newly discovered subpopulation of helper cd4+ t lymphocytes. it has been shown that these cells may contribute to tissue damage during certain inflammatory and autoimmune diseases and also play an important role in antitumor and antimicrobial, particularly antibacterial, immunity. bacteria stimulate the th17 response through several toll-like (tlr), nod-like (nlr) and c-type lectin (clr) receptors. when activated, th17 lymphocytes produce several cytokines, mainly int ... | 2015 | 25897100 |
| in vivo whole animal body imaging reveals colonization of chlamydia muridarum to the lower genital tract at early stages of infection. | the leading cause of sexually transmitted bacterial infection is chlamydia trachomatis. the aim of this study is to investigate the early events in colonization of this bacterium within the murine genital tract. | 2014 | 24723309 |
| lack of long-lasting hydrosalpinx in a/j mice correlates with rapid but transient chlamydial ascension and neutrophil recruitment in the oviduct following intravaginal inoculation with chlamydia muridarum. | lower genital tract infection with chlamydia trachomatis and c. muridarum can induce long-lasting hydrosalpinx in the upper genital tract of women and female mice, respectively. however, a/j mice were highly resistant to induction of long-lasting hydrosalpinx by c. muridarum. we further compared host inflammatory responses and chlamydial infection courses between the hydrosalpinx-resistant a/j mice and cba/j mice known to be susceptible to hydrosalpinx induction. both mouse strains developed rob ... | 2014 | 24711570 |
| the genetic basis of plasmid tropism between chlamydia trachomatis and chlamydia muridarum. | the development of genetic transformation technology for chlamydia trachomatis using its endogenous plasmid has recently been described. chlamydia muridarum cannot be transformed by the c. trachomatis plasmid, indicating a barrier between chlamydial species. to determine which regions of the plasmid conferred the species specificity, we used the novel approach of transforming wild-type c. muridarum carrying the endogenous plasmid pnigg and forced recombination with the c. trachomatis vector pgfp ... | 2014 | 24700815 |
| chlamydia muridarum infection-induced destruction of male germ cells and sertoli cells is partially prevented by chlamydia major outer membrane protein-specific immune cd4 cells. | chlamydia trachomatis infections are increasingly prevalent worldwide. male chlamydial infections are associated with urethritis, epididymitis, and orchitis; however, the role of chlamydia in prostatitis and male factor infertility remains controversial. using a model of chlamydia muridarum infection in male c57bl/6 mice, we investigated the effects of chlamydial infection on spermatogenesis and determined the potential of immune t cells to prevent infection-induced outcomes. antigen-specific cd ... | 2015 | 25472923 |
| plasmid-encoded pgp3 is a major virulence factor for chlamydia muridarum to induce hydrosalpinx in mice. | hydrosalpinx induction in mice by chlamydia muridarum infection, a model that has been used to study c. trachomatis pathogenesis in women, is known to depend on the cryptic plasmid that encodes eight genes designated pgp1 to pgp8. to identify the plasmid-encoded pathogenic determinants, we evaluated c. muridarum transformants deficient in the plasmid-borne gene pgp3, -4, or -7 for induction of hydrosalpinx. c. muridarum transformants with an in-frame deletion of either pgp3 or -4 but not -7 fail ... | 2014 | 25287930 |
| the mucosal expression pattern of interferon-ε in rhesus macaques. | type i ifns play an important role in innate and adaptive immunity against viral infections. a novel type i ifn, namely ifn-ε, which can protect against vaginal transmission of hsv2 and chlamydia muridarum bacterial infection, has been described in mice and humans. nevertheless, the principle cell type and the expression pattern of ifn-ε in tissues remain uncertain. in addition, the expression of ifn-ε in indian rhesus macaques (macaca mulatta) has not been reported. here, we analyzed ifn-ε expr ... | 2014 | 25139290 |
| reply to letter to the editor re: "in vivo whole animal body imaging reveals colonization of chlamydia muridarum to the lower genital tract at early stages of infection". | | 2014 | 25082537 |
| letter to the editor re: in vivo whole animal body imaging reveals colonization of chlamydia muridarum to the lower genital tract at early stages of infection. | | 2014 | 25080324 |
| protection promoted by pgp3 or pgp4 against chlamydia muridarum is mediated by cd4(+) cells in c57bl/6n mice. | urogenital tract infection with chlamydia trachomatis is a leading cause of sexually transmitted infections. there is currently no commercially available vaccine against c. trachomatis. the highly conserved plasmid of chlamydiae has been considered to be a virulence factor and the plasmid proteins have important roles in the chlamydia-specific immune response. this study was designed to evaluate the efficacy of vaccination with plasmid proteins in the prevention of c. muridarum lung infection in ... | 2014 | 25077421 |
| bioluminescence imaging of chlamydia muridarum ascending infection in mice. | chlamydial pathogenicity in the upper genital tract relies on chlamydial ascending from the lower genital tract. to monitor chlamydial ascension, we engineered a luciferase-expressing c. muridarum. in cells infected with the luciferase-expressing c. muridarum, luciferase gene expression and enzymatic activity (measured as bioluminescence intensity) correlated well along the infection course, suggesting that bioluminescence can be used for monitoring chlamydial replication. following an intravagi ... | 2014 | 24983626 |
| chlamydia muridarum infection associated host micrornas in the murine genital tract and contribution to generation of host immune response. | chlamydia trachomatis (ct) is the leading sexually transmitted bacterial infection in humans and is associated with reproductive tract damage. however, little is known about the involvement and regulation of micrornas (mirs) in genital ct. | 2015 | 24976530 |
| early microrna expression profile as a prognostic biomarker for the development of pelvic inflammatory disease in a mouse model of chlamydial genital infection. | it is not currently possible to predict the probability of whether a woman with a chlamydial genital infection will develop pelvic inflammatory disease (pid). to determine if specific biomarkers may be associated with distinct chlamydial pathotypes, we utilized two chlamydia muridarum variants (c. muridarum var001 [cmvar001] and cmvar004) that differ in their abilities to elicit upper genital tract pathology in a mouse model. cmvar004 has a lower growth rate in vitro and induces pathology in onl ... | 2014 | 24961692 |
| benzylidene acylhydrazides inhibit chlamydial growth in a type iii secretion- and iron chelation-independent manner. | chlamydiae are widespread gram-negative pathogens of humans and animals. salicylidene acylhydrazides, developed as inhibitors of type iii secretion system (t3ss) in yersinia spp., have an inhibitory effect on chlamydial infection. however, these inhibitors also have the capacity to chelate iron, and it is possible that their antichlamydial effects are caused by iron starvation. therefore, we have explored the modification of salicylidene acylhydrazides with the goal to uncouple the antichlamydia ... | 2014 | 24914180 |
| complement factor c5 but not c3 contributes significantly to hydrosalpinx development in mice infected with chlamydia muridarum. | hydrosalpinx is a pathological hallmark of tubal infertility associated with chlamydial infection. however, the mechanisms of hydrosalpinx remain unknown. here, we report that complement factor 5 (c5) contributes significantly to chlamydial induction of hydrosalpinx. mice lacking c5 (c5(-/-)) failed to develop any hydrosalpinx, while ∼42% of the corresponding wild-type mice (c5(+/+)) did so following intravaginal infection with chlamydia muridarum. surprisingly, deficiency in c3 (c3(-/-)), an up ... | 2014 | 24842924 |
| increased immunoaccessibility of momp epitopes in a vaccine formulated with amphipols may account for the very robust protection elicited against a vaginal challenge with chlamydia muridarum. | there is a need to implement a vaccine to protect against chlamydia trachomatis infections. to test a new vaccine, mice were immunized with the chlamydia muridarum native major outer membrane protein (nmomp) solubilized with either amphipol a8-35 or the detergent z3-14. ova was used as a negative control, and mice were inoculated intranasally with c. muridarum as positive controls. animals vaccinated with nmomp mounted strong chlamydia-specific humoral and cell-mediated immune responses. mice va ... | 2014 | 24778450 |
| induction of the chlamydia muridarum stress/persistence response increases azithromycin treatment failure in a murine model of infection. | viable but noninfectious (stressed/persistent) chlamydiae are more resistant to azithromycin (azm) in culture than are organisms in the normal developmental cycle. chlamydia muridarum-infected mice were exposed to amoxicillin to induce the organisms to enter the persistent/stressed state and subsequently treated with azm. azm treatment failure was observed in 22% of persistently infected mice, with an average of 321,667 inclusion-forming units (ifu) shed after azm treatment. productively infecte ... | 2014 | 24342653 |
| il-17e production is elevated in the lungs of balb/c mice in the later stages of chlamydia muridarum infection and re-infection. | pathogens can influence allergic respiratory diseases. we previously found that multiple infections with chlamydophila pneumoniae induce the production of interleukin-17a (il-17a) and il-17e, which have roles in the pathogenesis of asthma. the present work was designed to investigate our hypothesis that infections with another pathogen can induce the production of il-17a and il-17e. | 2016 | 24292583 |
| il-23 induces il-22 and il-17 production in response to chlamydia muridarum genital tract infection, but the absence of these cytokines does not influence disease pathogenesis. | chlamydia trachomatis infections are a significant cause of reproductive tract pathology. protective and pathological immune mediators must be differentiated to design a safe and effective vaccine. | 2013 | 24238108 |
| induction of protective immunity against chlamydia muridarum intracervical infection in dba/1j mice. | we previously reported that intracervical inoculation with chlamydia muridarum induced hydrosalpinx in dba/1j mice, but intravaginal inoculation failed to do so. in the current study, we found unexpectedly that intrabursal inoculation of live chlamydial organisms via the oviduct failed to induce significant hydrosalpinx. we further tested whether primary infection via intravaginal or intrabursal inoculation could induce protective immunity against hydrosalpinx following intracervical challenge i ... | 2014 | 24188757 |
| target cell limitation constrains chlamydial load in persistent infections: results from mathematical modelling applied to mouse genital tract infection data. | the interactions between chlamydial pathogens and their host contribute to the outcome of infection. nonresolving infections in immunodeficient mice can provide insights into these mechanisms by allowing observation of a form of persistent infection. using a mathematical model, we predict that in a nonresolving infection, the number of chlamydiae in the host will attain a stable equilibrium and that this equilibrium will be independent of the inoculum size. we test this hypothesis by infecting r ... | 2015 | 25044245 |
| evaluation of a multisubunit recombinant polymorphic membrane protein and major outer membrane protein t cell vaccine against chlamydia muridarum genital infection in three strains of mice. | an efficacious vaccine is needed to control chlamydia trachomatis infection. in the murine model of chlamydia muridarum genital infection, multifunctional mucosal cd4 t cells are the foundation for protective immunity, with antibody playing a secondary role. we previously identified four chlamydia outer membrane proteins (pmpe, pmpf, pmpg and pmph) as cd4 t cell vaccine candidates using a dendritic cell-based immunoproteomic approach. we also demonstrated that these four polymorphic membrane pro ... | 2014 | 24992718 |
| cd43-, but not cd43+, il-10-producing cd1dhicd5+ b cells suppress type 1 immune responses during chlamydia muridarum genital tract infection. | regulatory b (breg) cells are known to modulate immune responses through predominantly interleukin-10 (il-10)-dependent mechanisms and can be hypothetically divided into innate and adaptive subsets based on the nature of their activating signals. however, the specific role of different breg subsets in modulating immune responses remains ambiguous. here we have shown that chlamydia induces il-10-producing splenic b-cell populations consisting of cd43(+) and cd43(-) subsets of igm(hi)igd(lo) innat ... | 2015 | 24938746 |
| steroids alone or as adjunctive therapy with doxycycline fail to improve oviduct damage in mice infected with chlamydia muridarum. | in women, chlamydia trachomatis can ascend from the cervix to the fallopian tubes, where an overly aggressive host inflammatory response can cause scarring that leads to chronic pelvic pain, infertility, or ectopic pregnancy. although screening and treatment programs for women have resulted in decreased rates of sequelae, morbidities associated with oviduct scarring continue to occur. since corticosteroids have anti-inflammatory and antifibrotic effects, we tested the ability of dexamethasone to ... | 2014 | 24695778 |
| expression of chlamydia muridarum plasmid genes and immunogenicity of pgp3 and pgp4 in different mouse strains. | chlamydia muridarum carries a cryptic plasmid (pmopn) of 7.5kb, which encodes seven genes. our aims were to describe the transcriptional pattern of the pmopn genes in c. muridarum-infected mice and to evaluate the host immune responses against pgp3 and pgp4 proteins. balb/c and c57bl/6n female mice were inoculated intranasally with c. muridarum and sacrificed at different time points, and the total rna was extracted from the lung suspensions to determine the levels of expression of the different ... | 2014 | 24631212 |
| enhanced inducible costimulator ligand (icos-l) expression on dendritic cells in interleukin-10 deficiency and its impact on t-cell subsets in respiratory tract infection. | an association between inducible costimulator ligand (icos-l) expression and interleukin (il)-10 production by dendritic cells (dcs) has been commonly found in infectious disease. dcs with higher icos-l expression and il-10 production are reportedly more efficient in inducing regulatory t cells (tregs). here we use the chlamydia muridarum (cm) lung infection model in il-10 knockout (ko) mice to test the relationship between il-10 production and icos-l expression by dcs. we examined icos-l expres ... | 2013 | 24100657 |
| the duration of chlamydia muridarum genital tract infection and associated chronic pathological changes are reduced in il-17 knockout mice but protection is not increased further by immunization. | il-17 is believed to be important for protection against extracellular pathogens, where clearance is dependent on neutrophil recruitment and local activation of epithelial cell defences. however, the role of il-17 in protection against intracellular pathogens such as chlamydia is less clear. we have compared (i) the course of natural genital tract c. muridarum infection, (ii) the development of oviduct pathology and (iii) the development of vaccine-induced immunity against infection in wild type ... | 2013 | 24073293 |
| cd4+ t cell expression of myd88 is essential for normal resolution of chlamydia muridarum genital tract infection. | resolution of chlamydia genital tract infection is delayed in the absence of myd88. in these studies, we first used bone marrow chimeras to demonstrate a requirement for myd88 expression by hematopoietic cells in the presence of a wild-type epithelium. using mixed bone marrow chimeras we then determined that myd88 expression was specifically required in the adaptive immune compartment. furthermore, adoptive transfer experiments revealed that cd4(+) t cell expression of myd88 was necessary for no ... | 2013 | 24038087 |
| cd1d-restricted nkt cells modulate placental and uterine leukocyte populations during chlamydial infection in mice. | invariant cd1d-restricted natural killer t cells play an important immunoregulatory role and can influence a broad spectrum of immunological responses including against bacterial infections. they are present at the fetal-maternal interface and although it has been reported that experimental systemic inkt cell activation can induce mouse abortion, their role during pregnancy remain poorly understood. in the present work, using a physiological chlamydia muridarum infection model, we have shown tha ... | 2013 | 23999314 |
| intracellular survival and persistence of chlamydia muridarum is determined by macrophage polarization. | macrophages can display a number of distinct phenotypes, known collectively as polarized macrophages. the best defined of these phenotypes are the classically-activated, interferon gamma (ifnγ)/lps induced (m1) and alternatively-activated, il-4 induced (m2) macrophages. the goal of this study is to characterize macrophage-chlamydia interactions in the context of macrophage polarization. here we use chlamydia muridarum and murine bone-marrow derived macrophages to show chlamydia does not induce m ... | 2013 | 23967058 |
| cd4⁺cd25⁺foxp3⁺ regulatory t cells promote th17 responses and genital tract inflammation upon intracellular chlamydia muridarum infection. | the functional role of cd4⁺cd25⁺foxp3⁺ regulatory t cells (tregs) in host responses to intracellular bacterial infection was investigated in an in vitro coculturing system and a murine model of chlamydia muridarum genital tract infection. remarkably, c. muridarum infection subverted the immune suppressive role of cd4⁺cd25⁺foxp3⁺ tregs; instead of hampering immune responses, tregs not only promoted th17 differentiation from conventional cd4⁺ t cells but also themselves converted into proinflammat ... | 2013 | 23956419 |
| chlamydia muridarum enters a viable but non-infectious state in amoxicillin-treated balb/c mice. | in culture, exposure to penicillin and other stressors induce chlamydiae to enter a non-infectious but viable state termed persistence. chlamydiae may reenter their normal developmental cycle after stressor removal. though aberrant rb similar to those present in culture models of persistence have been observed within infected tissues, the existence of persistent chlamydiae has not been definitively demonstrated in vivo. as a result, the role of persistent organisms in pathogenesis is undefined. ... | 2012 | 22943883 |
| oviduct infection and hydrosalpinx in dba1/j mice is induced by intracervical but not intravaginal inoculation with chlamydia muridarum. | intravaginal infection with c. muridarum in mice often results in hydrosalpinx similar to that found in women urogenitally infected with c. trachomatis, making the c. muridarum lower genital tract infection murine model suitable for studying c. trachomatis pathogenesis. to our surprise, dba1/j mice were highly resistant to hydrosalpinx following an intravaginal infection with c. muridarum although these mice were as susceptible to lower genital tract infection as other mouse strains. a significa ... | 2013 | 23940777 |
| chlamydia trachomatis infection of the male genital tract: an update. | chlamydia trachomatis (ct) is the most prevalent cause of sexually transmitted diseases. although the prevalence of chlamydial infection is similar in men and women, current research and screening are still focused on women, who develop the most severe complications, leaving the study of male genital tract (mgt) infection underrated. herein, we reviewed the literature on genital ct infection with special focus on the mgt. data indicate that ct certainly infects different parts of the mgt such as ... | 2013 | 23870458 |
| chlamydial infection of the gastrointestinal tract: a reservoir for persistent infection. | the mechanism by which chlamydiae persist in vivo remains undefined; however, chlamydiae in most animals persist in the gastrointestinal tract (gi) and are transmitted via the fecal-oral route. oral infection of mice with chlamydia muridarum was previously shown to establish a long-term persistent infection in the gi tract. in this study, balb/c, dba/2, and c57bl/6 mice, infected orally with c. muridarum, were infected in the cecum for as long as 100 days in the absence of pathology. the primary ... | 2013 | 23843274 |
| reduced live organism recovery and lack of hydrosalpinx in mice infected with plasmid-free chlamydia muridarum. | plasmid-free chlamydia trachomatis and chlamydia muridarum fail to induce severe pathology. to evaluate whether the attenuated pathogenicity is due to insufficient infection or inability of the plasmidless chlamydial organisms to trigger pathological responses, we compared plasmid-competent and plasmid-free c. muridarum infections in 5 different strains of mice. all 5 strains developed hydrosalpinx following intravaginal inoculation with plasmid-competent, but not inoculation with plasmid-free, ... | 2014 | 24343644 |
| identification of a serine protease inhibitor which causes inclusion vacuole reduction and is lethal to chlamydia trachomatis. | the mechanistic details of the pathogenesis of chlamydia, an obligate intracellular pathogen of global importance, have eluded scientists due to the scarcity of traditional molecular genetic tools to investigate this organism. here we report a chemical biology strategy that has uncovered the first essential protease for this organism. identification and application of a unique cthtra inhibitor (jo146) to cultures of chlamydia resulted in a complete loss of viable elementary body formation. jo146 ... | 2013 | 23796320 |
| contribution of interleukin-12 p35 (il-12p35) and il-12p40 to protective immunity and pathology in mice infected with chlamydia muridarum. | the p35 molecule is unique to interleukin-12 (il-12), while p40 is shared by both il-12 and il-23. il-12 promotes th1 t cell responses, while il-23 promotes th17 t cell responses. the roles of il-12p35- and il-12p40-mediated responses in chlamydial infection were compared in mice following an intravaginal infection with chlamydia muridarum. mice deficient in either il-12p35 or p40 both developed similar but prolonged infection time courses, confirming the roles of il-12-mediated immune responses ... | 2013 | 23753624 |
| endosulfatases sulf1 and sulf2 limit chlamydia muridarum infection. | the first step in attachment of chlamydia to host cells is thought to involve reversible binding to host heparan sulfate proteoglycans (hspgs), polymers of variably sulfated repeating disaccharide units coupled to diverse protein backbones. however, the key determinants of hspg structure that are involved in chlamydia binding are incompletely defined. a previous genome-wide drosophila rnai screen suggested that the level of hspg 6-o sulfation rather than the identity of the proteoglycan backbone ... | 2013 | 23480519 |
| interferon-ε protects the female reproductive tract from viral and bacterial infection. | the innate immune system senses pathogens through pattern-recognition receptors (prrs) that signal to induce effector cytokines, such as type i interferons (ifns). we characterized ifn-ε as a type i ifn because it signaled via the ifnar1 and ifnar2 receptors to induce ifn-regulated genes. in contrast to other type i ifns, ifn-ε was not induced by known prr pathways; instead, ifn-ε was constitutively expressed by epithelial cells of the female reproductive tract (frt) and was hormonally regulated ... | 2013 | 23449591 |
| innate immunity is sufficient for the clearance of chlamydia trachomatis from the female mouse genital tract. | chlamydia muridarum and chlamydia trachomatis, mouse and human strains, respectively, have been used to study immunity in a murine model of female genital tract infection. despite evidence that unique genes of these otherwise genomically similar strains could play a role in innate immune evasion in their respective mouse and human hosts, there have been no animal model findings to directly support this conclusion. here, we infected c57bl/6 and adaptive immune-deficient rag1(-/-) female mice with ... | 2014 | 24585717 |
| intranasal vaccination with chlamydia pneumoniae induces cross-species immunity against genital chlamydia muridarum challenge in mice. | chlamydia trachomatis is the most common bacterial sexually transmitted disease in the world and specifically in the united states, with the highest incidence in age-groups 14-19 years. in a subset of females, the c. trachomatis genital infection leads to serious pathological sequelae including pelvic inflammatory disease, ectopic pregnancy, and infertility. chlamydia pneumoniae, another member of the same genus, is a common cause of community acquired respiratory infection with significant numb ... | 2013 | 23741420 |
| perforin is detrimental to controlling [corrected] c. muridarum replication in vitro, but not in vivo. | cd4 t cells are critical for clearing experimental chlamydia muridarum genital tract infections. two independent in vitro cd4 t cell mechanisms have been identified for terminating chlamydia replication in epithelial cells. one mechanism, requiring ifn-γ and t cell-epithelial cell contact, terminates infection by triggering epithelial production of nitric oxide to chlamydiacidal levels; the second is dependent on t cell degranulation. we recently demonstrated that there are two independent in vi ... | 2013 | 23691028 |
| induction of protective immunity against chlamydia muridarum intravaginal infection with the chlamydial immunodominant antigen macrophage infectivity potentiator. | we previously reported that 5 chlamydia muridarum antigens reacted with antisera from >90% mice urogenitally infected with c. muridarum and they are tc0660 (abc transporter or artj), tc0727 (outer membrane complex protein b or omcb), tc0828 (macrophage infectivity potentiator or mip), tc0726 (inclusion membrane protein or inc) & tc0268 (hypothetical protein or hp). the orthologs of these antigens in chlamydia trachomatis were also highly reactive with antisera from women urogenitally infected wi ... | 2013 | 23416214 |
| characterization of in vitro chlamydia muridarum persistence and utilization in an in vivo mouse model of chlamydia vaccine. | chlamydia trachomatis genital tract infections are easily treated with antibiotics; however, the majority of infections are asymptomatic and therefore untreated, highlighting the need for a vaccine. because most infections are asymptomatic, vaccination could potentially be administered to individuals who may have an acute infection at that time. in such individuals, the effect of vaccination on the existing infection is unknown; however, one potential outcome could be the development of a persis ... | 2013 | 23414449 |
| usefulness of 11c-choline positron emission tomography for genital chlamydial infection assessment in a balb/c murine model. | the aim of this study is to explore the feasibility of 11c-choline pet in the assessment of the degree of inflammation in the chlamydia muridarum genital infection model. | 2013 | 23362001 |
| chlamydial infection in vitamin d receptor knockout mice is more intense and prolonged than in wild-type mice. | vitamin d hormone (1,25-dihydroxyvitamin d) is involved in innate immunity and induces host defense peptides in epithelial cells, suggesting its involvement in mucosal defense against infections. chlamydia trachomatis is a major cause of bacterial sexually transmitted disease worldwide. we tested the hypothesis that the vitamin d endocrine system would attenuate chlamydial infection. vitamin d receptor knock-out mice (vdr(-/-)) and wild-type mice (vdr(+/+)) were infected with 10(3) inclusion for ... | 2013 | 23201171 |
| mechanism of t-cell mediated protection in newborn mice against a chlamydia infection. | to determine the immune components needed for protection of newborn mice against chlamydia muridarum, animals born to chlamydia-immunized and to sham-immunized dams were infected intranasally with c. muridarum at 2 post-natal days. t-cells isolated from immunized or sham-immunized adult mice were adoptively transferred to newborn mice at the time of infection. also, to establish what cytokines are involved in protection, ifn-γ, tnf-α, il-10, and il-12 were passively transferred to newborn mice. ... | 2017 | 23644176 |
| ot-1 mice display minimal upper genital tract pathology following primary intravaginal chlamydia muridarum infection. | chlamydia trachomatis is the most common bacterial sexually transmitted disease worldwide and leads to serious pathological sequelae in the upper genital tract (ugt) including pelvic inflammatory disease, ectopic pregnancy, and infertility. several components of the host immune responses have been shown to contribute to the ugt pathology following genital chlamydial infection. we have shown recently that cd8(+) t cells induce the chlamydial ugt pathology via the production of tnf-α. however, tho ... | 2013 | 23620186 |
| interruption of cxcl13-cxcr5 axis increases upper genital tract pathology and activation of nkt cells following chlamydial genital infection. | regulation of immune responses is critical for controlling inflammation and disruption of this process can lead to tissue damage. we reported that cxcl13 was induced in fallopian tube tissue following c. trachomatis infection. here, we examined the influence of the cxcl13-cxcr5 axis in chlamydial genital infection. | 2012 | 23189125 |
| signaling via tumor necrosis factor receptor 1 but not toll-like receptor 2 contributes significantly to hydrosalpinx development following chlamydia muridarum infection. | chlamydial infection in the lower genital tract can lead to hydrosalpinx, which is accompanied by activation of both pattern recognition receptor tlr2- and inflammatory cytokine receptor tnfr1-mediated signaling pathways. in the current study, we compared the relative contributions of these two receptors to chlamydial induction of hydrosalpinx in mice. we found that mice with or without deficiencies in tlr2 or tnfr1 displayed similar time courses of live organism shedding from vaginal swabs, sug ... | 2014 | 24549331 |
| divergent outcomes following transcytosis of igg targeting intracellular and extracellular chlamydial antigens. | antibodies can have a protective but non-essential role in natural chlamydial infections dependent on antigen specificity and antibody isotype. igg is the dominant antibody in both male and female reproductive tract mucosal secretions, and is bi-directionally trafficked across epithelia by the neonatal fc receptor (fcrn). using ph-polarized epididymal epithelia grown on transwells, igg specifically targeted at an extracellular chlamydial antigen; the major outer membrane protein (momp), enhanced ... | 2017 | 24445600 |
| ifn-ε is constitutively expressed by cells of the reproductive tract and is inefficiently secreted by fibroblasts and cell lines. | type-i interferons (ifns) form a large family of cytokines that primarily act to control the early development of viral infections. typical type-i ifn genes, such as those encoding ifn-α or ifn-β are upregulated by viral infection in many cell types. in contrast, the gene encoding ifn-ε was reported to be constitutively expressed by cells of the female reproductive tract and to contribute to the protection against vaginal infections with herpes simplex virus 2 and chlamydia muridarum. our data c ... | 2013 | 23951133 |
| [relationship between cd4 + cd25 + foxp3 + regulatory t cells and th17 responses in chlamydia muridarum pulmonary infection]. | to study the relationship between cd4 + cd25 + foxp3 + regulatory t cells and th17 responses during pulmonary infection of chlamydia muridarum (cm) in balb/c mice. [methods] balb/c mice aged 6-8 weeks were inoculated intranasally with 5 x 103 ifu of cm to set up the murine model of chlamydial pneumonia. the boet weight changes, the growth of cm and the pathology in the lung were monitored at different time post-infection. in determine the cd4 + cd25 + foxp3 + regulatory t cells responses in balb ... | 2013 | 23614243 |
| an atypical cd8 t-cell response to chlamydia muridarum genital tract infections includes t cells that produce interleukin-13. | chlamydia trachomatis urogenital serovars d-k are intracellular bacterial pathogens that replicate almost exclusively in human reproductive tract epithelium. in the c. muridarum mouse model for human chlamydia genital tract infections cd4 t helper type 1 cell responses mediate protective immunity while cd8 t-cell responses have been associated with scarring and infertility. scarring mediated by cd8 t cells requires production of tumour necrosis factor-α (tnf-α); however, tnf-α is associated with ... | 2014 | 24428415 |
| transformation of chlamydia muridarum reveals a role for pgp5 in suppression of plasmid-dependent gene expression. | transformation of chlamydia trachomatis should greatly advance the chlamydial research. however, significant progress has been hindered by the failure of c. trachomatis to induce clinically relevant pathology in animal models. chlamydia muridarum, which naturally infects mice, can induce hydrosalpinx in mice, a tubal pathology also seen in women infected with c. trachomatis. we have developed a c. muridarum transformation system and confirmed pgp1, -2, -6, and -8 as plasmid maintenance factors, ... | 2014 | 24363344 |
| from mice to women and back again: causalities and clues for chlamydia-induced tubal ectopic pregnancy. | to provide an overview of knockout mouse models that have pathological tubal phenotypes after chlamydia muridarum infection, discuss factors and pathological processes that contribute to inflammation, summarize data on tubal transport and progression of tubal implantation from studies in humans and animal models, and highlight research questions in the field. | 2012 | 22884019 |
| chlamydia muridarum lung infection in infants alters hematopoietic cells to promote allergic airway disease in mice. | viral and bacterial respiratory tract infections in early-life are linked to the development of allergic airway inflammation and asthma. however, the mechanisms involved are not well understood. we have previously shown that neonatal and infant, but not adult, chlamydial lung infections in mice permanently alter inflammatory phenotype and physiology to increase the severity of allergic airway disease by increasing lung interleukin (il)-13 expression, mucus hyper-secretion and airway hyper-respon ... | 2012 | 22870337 |
| il-17a synergizes with ifn-γ to upregulate inos and no production and inhibit chlamydial growth. | ifn-γ-mediated inducible nitric oxide synthase (inos) expression is critical for controlling chlamydial infection through microbicidal nitric oxide (no) production. interleukin-17a (il-17a), as a new proinflammatory cytokine, has been shown to play a protective role in host defense against chlamydia muridarum (cm) infection. to define the related mechanism, we investigated, in the present study, the effect of il-17a on ifn-γ induced inos expression and no production during cm infection in vitro ... | 2012 | 22745717 |
| tlr2, but not tlr4, is required for effective host defence against chlamydia respiratory tract infection in early life. | chlamydia pneumoniae commonly causes respiratory tract infections in children, and epidemiological investigations strongly link infection to the pathogenesis of asthma. the immune system in early life is immature and may not respond appropriately to pathogens. toll-like receptor (tlr)2 and 4 are regarded as the primary pattern recognition receptors that sense bacteria, however their contribution to innate and adaptive immunity in early life remains poorly defined. we investigated the role of tlr ... | 2012 | 22724018 |