Detection of Chlamydia trachomatis in Fallopian tube tissue in women with postinfectious tubal infertility
Biopsy tissues from women with postinfectious tubal infertility were studied for the presence of Chlamydia trachomatis.
Tubal biopsy specimens from 25 women with postinfectious tubal infertility undergoing laparoscopy for repair of fallopian tubes were evaluated by culture, in situ hybridization. Immunocytochemistry, and transmission electron microscopy for the presence of Chlamydia trachomatis. Serum was also tested for Chlamydia trachomatis antibodies.
Chlamydia trachomatis was detected in postinfectious tubal biopsy specimens in three of 25 patients by culture, 12 of 24 by in situ hybridization, 15 of 22 by immunoperoxidase stain, and two of 10 by transmission electron microscopy. Serum antibody against Chlamydia trachomatis was detected in 15 of 21 patients.
Chlamydia trachomatis deoxyribonucleic acid or antigens were detected at a high percentage (19/24 women) in the biopsy tissues of the fimbrial and peritubal adhesions by in situ hybridization or immunoperoxidase stain, suggesting a persistent infection in these women even after antibiotic treatment.
Available from: Robert Schoborg
- "Notably, the persistent chlamydiae can re-enter and complete the normal developmental cycle once the " inducer " is removed. Several studies suggest that under appropriate circumstances, chlamydial persistence may occur in vivo in humans (Patton et al., 1994; Fortenberry et al., 1999; Dean et al., 2000; Bragina et al., 2001; Gerard et al., 2001). Recently, persistence induction in vivo has been definitively demonstrated using a murine model of amoxicillin-induced C. muridarum persistence (Phillips Campbell et al., 2012). "
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ABSTRACT: Interaction of Herpes Simplex Virus (HSV) glycoprotein D (gD) with the host cell surface during Chlamydia trachomatis/HSV co-infection stimulates chlamydiae to become persistent. During viral entry, gD interacts with one of 4 host co-receptors: HVEM (herpes virus entry mediator), nectin-1, nectin-2 and 3-O-sulfated heparan sulfate. HVEM and nectin-1 are high-affinity entry receptors for both HSV-1 and HSV-2. Nectin-2 mediates HSV-2 entry but is inactive for HSV-1, while 3-O-sulfated heparan sulfate facilitates HSV-1, but not HSV-2, entry. Western blot and RT-PCR analyses demonstrate that HeLa and HEC-1B cells express nectin-1 and nectin-2, but not HVEM. Because both HSV-1 and HSV-2 trigger persistence, these data suggest that nectin-1 is the most likely co-receptor involved. Co-infections with nectin-1 specific HSV-1 mutants stimulate chlamydial persistence, as evidenced by aberrant body (AB) formation and decreased production of elementary bodies (EBs). These data indicate that nectin-1 is involved in viral-induced chlamydial persistence. However, inhibition of signal transduction molecules associated with HSV attachment and entry does not rescue EB production during C. trachomatis/HSV-2 co-infection. HSV attachment also does not activate Cdc42 in HeLa cells, as would be expected with viral stimulated activation of nectin-1 signaling. Additionally, immunofluorescence assays confirm that HSV infection decreases nectin-1 expression. Together, these observations suggest that gD binding-induced loss of nectin-1 signaling negatively influences chlamydial growth. Chlamydial infection studies in nectin-1 knockdown (NKD) HeLa cell lines support this hypothesis. In NKD cells, chlamydial inclusions are smaller in size, contain ABs, and produce significantly fewer infectious EBs compared to C. trachomatis infection in control HeLa cells. Overall, the current study indicates that the actions of host molecule, nectin-1, are required for successful C. trachomatis development.
Available from: Paola Mastromarino
- "The ability of C. trachomatis to develop into a persistent form has been suggested as key pathogenetic mechanism underlying chronic infections (Beatty et al., 1994; Dean et al., 2000). In particular, persistent C. trachomatis forms may be involved in the pathogenesis of severe sequelae since they may act as chronic stimulus leading to chronic inflammatory state and subsequent tissue damage (Ness et al., 2008; Patton et al., 1994). Similarly, persistent forms may also explain infections that recur despite appropriate antichlamydial therapy (Batteiger et al., 2010; Bragina et al., 2001; Dean et al., 2000). "
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ABSTRACT: Increasing evidence indicates that abnormal vaginal flora lacking lactobacilli facilitates the acquisition of several sexually transmitted diseases including Chlamydia trachomatis. C. trachomatis, the most common bacterial agent of genital infections worldwide, can progress from the lower to upper reproductive tract and induce severe sequelae. The ability of C. trachomatis to develop into a persistent form has been suggested as key pathogenetic mechanism underlying chronic infections and sequelae. The aim of our study was to investigate the C. trachomatis interaction with vaginal microbiota analyzing the effects of Lactobacillus strains (L. brevis and L. salivarius) on the different phases of C. trachomatis developmental cycle. In addition, the effect of lactobacilli on persistent chlamydial forms induced by HSV-2 coinfection has also been evaluated. Our results demonstrated significant inhibition of C. trachomatis multiplication by vaginal lactobacilli. L. brevis was significantly more effective than L. salivarius (p < 0.05) on all the steps of chlamydial infection cycle suggesting that the ability of lactobacilli to protect from infection is strain-dependent. Lactobacilli had an adverse effect on elementary chlamydial bodies (p < 0.05), on chlamydial adsorption to epithelial cells (p < 0.001) and on intracellular phases of chlamydial replication (p < 0.0001). Our study also demonstrated a protective effect of lactobacilli towards persistent C. trachomatis forms induced by HSV-2 coinfection. A significant increase in the production of C. trachomatis infectious progeny was observed in C. trachomatis/HSV-2 coinfection in the presence of L. brevis (p = 0.01) despite a significant inhibition of C. trachomatis multiplication (p = 0.028). Our data suggest that a healthy vaginal microbiota can reduce the risk of acquiring C. trachomatis infection and counteract the development of persistent chlamydial forms.
Available from: Lyndsey Buckner
- "Of these, varying levels of IFNγ in the endocervix during chlamydial infection in vivo are likely crucial as demonstrated by studies in vitro, in animal models, and in observational studies in humans (Arno et al., 1990; Beatty et al., 1994a; Byrne, 2001; Aiyar et al., 2014; Lewis et al., 2014). The direct involvement of persistent growth forms in pathogenesis in vivo in humans is challenging to prove, but several TEM studies have visualized atypical pleomorphic RBs and aberrant C. trachomatis forms in individuals with chronic infections, in Fallopian tube tissues, and in the synovium of reactive arthritis patients (Patton et al., 1994; Nanagara et al., 1995; Mazzoli et al., 2000; Bragina et al., 2001). Very recently, the Quayle laboratory developed methodology to sample endocervical cells and components of the endocervical environment in C. trachomatis infected women. "
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ABSTRACT: Bacteria have evolved specific adaptive responses to cope with changing environments. These adaptations include stress response phenotypes with dynamic modifications of the bacterial cell envelope and generation of membrane vesicles (MVs). The obligate intracellular bacterium, Chlamydia trachomatis, typically has a biphasic lifestyle, but can enter into an altered growth state typified by morphologically aberrant chlamydial forms, termed persistent growth forms, when induced by stress in vitro. How C. trachomatis can adapt to a persistent growth state in host epithelial cells in vivo is not well understood, but is an important question, since it extends the host-bacterial relationship in vitro and has thus been indicated as a survival mechanism in chronic chlamydial infections. Here, we review recent findings on the mechanistic aspects of bacterial adaptation to stress with a focus on how C. trachomatis remodels its envelope, produces MVs, and the potential important consequences of MV production with respect to host-pathogen interactions. Emerging data suggest that the generation of MVs may be an important mechanism for C. trachomatis intracellular survival of stress, and thus may aid in the establishment of a chronic infection in human genital epithelial cells.
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