The mucosal immune response to Chlamydia trachomatis infection of the reproductive tract in women

Agrawal, Tanvi; Vats, Vikas; Salhan, Sudha; Mittal, Aliza

doi:10.1016/j.jri.2009.07.013

Cited by 35 publications

(39 citation statements)

References 33 publications

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“…Little is known about the presence of local Chlamydia antibodies in the cervicovaginal mucosa. The dominant Chlamydia antibody in cervicovaginal fluid is IgG rather than IgA [31]. In women with a current Chlamydia infection, presence of combined Ct IgMAG antibodies was recorded in 83% and IgA in 38% [18]; interestingly IgA showed a clear (inverse) correlation with the number of bacteria detected in the cervical secretions tested.…”

Section: Discussionmentioning

confidence: 99%

Chlamydia trachomatisAntibody Testing in Vaginal Mucosal Material versus Blood Samples of Women Attending a Fertility Clinic and an STI Clinic

Broek

Land

Bergen

et al. 2014

Obstetrics and Gynecology International

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Background. Chlamydia infections often follow an asymptomatic course but may damage the reproductive tract. Chlamydia antibodies in serum are used as markers for past infections and can relate to tubal pathology and infertility. This “proof of principle” study aimed to assess whether Chlamydia antibodies are detectable in easier to obtain, noninvasive, vaginal mucosa samples and relate to current or past infection. Methods. We compared outcomes of Chlamydia IgG and IgA antibody tests in serum and vaginal mucosal swabs in (a) 77 women attending a fertility clinic, of whom 25 tested positive for serum-IgG and (b) 107 women visiting an STI centre, including 30 Chlamydia PCR-positive subjects. Results. In the STI clinic, active Chlamydia infections were linked to serum-IgG and serum-IgA (P < 0.001) and mucosa-IgA (P < 0.001), but not mucosa-IgG. In the fertility clinic, mucosa-IgG had stronger correlations with serum-IgG (P = 0.02) than mucosa-IgA (P = 0.06). Women with tubal pathology or Chlamydia history more commonly had serum-IgG and mucosa-IgA (both P < 0.001), whereas this link was weaker for mucosa-IgG (P = 0.03). Conclusion. Chlamydia IgG and IgA are detectable in vaginal mucosal material. Serum-IgG had stronger associations with current or past infections. Mucosa-IgA also showed associations with (past) infection and complications. IgA presence in vaginal mucosa warrants further epidemiological studies.

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Section: Discussionmentioning

confidence: 99%

Chlamydia trachomatisAntibody Testing in Vaginal Mucosal Material versus Blood Samples of Women Attending a Fertility Clinic and an STI Clinic

Broek

Land

Bergen

et al. 2014

Obstetrics and Gynecology International

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“…The presence of chlamydial EBs in the extracellular environment is readily recognized by components of the innate immune system (17). Toll-like receptors (TLRs) on all components of the innate immune system, including phagocytic cells and epithelial cells, especially TLR 2 and TLR 4, bind to pathogen-associated molecular patterns (PAMPs) on the surface of EBs and initiate the release of proinflammatory cytokines, as well as chemokines that attract immune cells to the site of infection (18).…”

Section: Immune Response To Infectionmentioning

confidence: 99%

Chlamydia trachomatis: the Persistent Pathogen

Witkin

Minis

Athanasiou

et al. 2017

Clin Vaccine Immunol

166

117

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Chlamydia trachomatis is an obligate intracellular bacterium whose only natural host is humans. Although presenting as asymptomatic in most women, genital tract chlamydial infections are a leading cause of pelvic inflammatory disease, tubal factor infertility, and ectopic pregnancy. C. trachomatis has evolved successful mechanisms to avoid destruction by autophagy and the host immune system and persist within host epithelial cells. The intracellular form of this organism, the reticulate body, can enter into a persistent nonreplicative but viable state under unfavorable conditions. The infectious form of the organism, the elementary body, is again generated when the immune attack subsides. In its persistent form, C. trachomatis ceases to produce its major structural and membrane components, but synthesis of its 60-kDa heat shock protein (hsp60) is greatly upregulated and released from the cell. The immune response to hsp60, perhaps exacerbated by repeated cycles of productive infection and persistence, may promote damage to fallopian tube epithelial cells, scar formation, and tubal occlusion. The chlamydial and human hsp60 proteins are very similar, and hsp60 is one of the first proteins produced by newly formed embryos. Thus, the development of immunity to epitopes in the chlamydial hsp60 that are also present in the corresponding human hsp60 may increase susceptibility to pregnancy failure in infected women. Delineation of host factors that increase the likelihood that C. trachomatis will avoid immune destruction and survive within host epithelial cells and utilization of this knowledge to design individualized preventative and treatment protocols are needed to more effectively combat infections by this persistent pathogen.

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“…TLR-dependent stimulation of FGT epithelial cells in vitro induces secretion of IL-1α, IL-1β, IL-6, IL-8 and TNF-α (64, 174), and cyclooxygenase 2 (COX-2), an inducible enzyme associated with mucosal inflammation (131), but few studies exist to support these findings in vivo . During infection by sexually transmitted pathogens, such as Chlamydia or Neisseria gonorrhoeae , secretion of IFN-γ, IL-10, IL-12, IL-1β, IL-6, and IL-8 has been reported in the cervix, fallopian tubes, and cervical secretions (174, 175). In the fallopian tubes and the uterus, the presence of endometrial epithelial cells, with similar functions than the intestinal M cells, favors secretion of inflammatory cytokines that can influence local immune responses (176).…”

Section: Tlr Expression and Responses In Human Mucosal Epithelial Tismentioning

confidence: 99%

TLR-Dependent Human Mucosal Epithelial Cell Responses to Microbial Pathogens

2014

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Toll-like receptor (TLR) signaling represents one of the best studied pathways to implement defense mechanisms against invading microbes in human being as well as in animals. TLRs respond to specific microbial ligands and to danger signals produced by the host during infection, and initiate downstream cascades that activate both innate and adaptive immunity. TLRs are expressed by professional immune cells and by the large majority of non-hematopoietic cells, including epithelial cells. In epithelial tissues, TLR functions are particularly important because these sites are constantly exposed to microorganisms, due to their location at the host interface with the environment. While at these sites specific defense mechanisms and inflammatory responses are initiated via TLR signaling against pathogens, suppression or lack of TLR activation is also observed in response to the commensal microbiota. The mechanisms by which TLR signaling is regulated in mucosal epithelial cells include differential expression and levels of TLRs (and their signaling partners), their cellular localization and positioning within the tissue in a fashion that favors responses to pathogens while dampening responses to commensals and maintaining tissue homeostasis in physiologic conditions. In this review, the expression and activation of TLRs in mucosal epithelial cells of several sites of the human body are examined. Specifically, the oral cavity, the ear canal and eye, the airways, the gut, and the reproductive tract are discussed, along with how site-specific host defense mechanisms are implemented via TLR signaling.

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The mucosal immune response to Chlamydia trachomatis infection of the reproductive tract in women

Cited by 35 publications

References 33 publications

Chlamydia trachomatisAntibody Testing in Vaginal Mucosal Material versus Blood Samples of Women Attending a Fertility Clinic and an STI Clinic

Chlamydia trachomatisAntibody Testing in Vaginal Mucosal Material versus Blood Samples of Women Attending a Fertility Clinic and an STI Clinic

Chlamydia trachomatis: the Persistent Pathogen

TLR-Dependent Human Mucosal Epithelial Cell Responses to Microbial Pathogens

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