Previously undetected Chlamydia trachomatis infection, immunity to heat shock proteins and tubal occlusion in women undergoing in-vitro fertilization

Spandorfer, S.D.

doi:10.1093/humrep/14.1.60

Cited by 47 publications

(23 citation statements)

References 14 publications

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“…A number of studies have shown that both humoral and cell-mediated immune responses to the chlamydial hsp60, as well as the generation of immune responses that recognize the human hsp60, contribute to the pathogenesis of a chlamydial genital tract infection (65)(66)(67)(68). It should be noted that when C. trachomatis was added to a fallopian tube organ culture, only minimal damage was noted (69).…”

Section: The C Trachomatis 60-kda Heat Shock Proteinmentioning

confidence: 99%

Chlamydia trachomatis: the Persistent Pathogen

Witkin

Minis

Athanasiou

et al. 2017

Clin Vaccine Immunol

165

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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Section: The C Trachomatis 60-kda Heat Shock Proteinmentioning

confidence: 99%

Chlamydia trachomatis: the Persistent Pathogen

Witkin

Minis

Athanasiou

et al. 2017

Clin Vaccine Immunol

165

117

View full text Add to dashboard Cite

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“…This has largely resulted from a body of literature demonstrating high-titer human antibody responses to cHSP60 in patients with tubal pathology and additionally that, in several animal models, tissue pathology developed after repeated inoculations with cHSP60 protein (reviewed in reference 138). However, this mechanism is a subject of considerable controversy because of inconsistencies between the different published findings, i.e., problems with protein preparations that involved a hypersensitive detergent being used in some animal models and cross-reactivity or poor specificity of some of the antibody tests (141)(142)(143)(144)(145)(146)(147). On the other hand, there is no doubt that cHSP60 is a predominant chlamydial antigen that does frequently elicit an immune response.…”

Section: Chsp60-induced Delayed Hypersensitivitymentioning

confidence: 99%

Human and Pathogen Factors Associated with Chlamydia trachomatis-Related Infertility in Women

et al. 2015

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SUMMARY Chlamydia trachomatis is the most common bacterial sexually transmitted pathogen worldwide. Infection can result in serious reproductive pathologies, including pelvic inflammatory disease, ectopic pregnancy, and infertility, in women. However, the processes that result in these reproductive pathologies have not been well defined. Here we review the evidence for the human disease burden of these chlamydial reproductive pathologies. We then review human-based evidence that links Chlamydia with reproductive pathologies in women. We present data supporting the idea that host, immunological, epidemiological, and pathogen factors may all contribute to the development of infertility. Specifically, we review the existing evidence that host and pathogen genotypes, host hormone status, age of sexual debut, sexual behavior, coinfections, and repeat infections are all likely to be contributory factors in development of infertility. Pathogen factors such as infectious burden, treatment failure, and tissue tropisms or ascension capacity are also potential contributory factors. We present four possible processes of pathology development and how these processes are supported by the published data. We highlight the limitations of the evidence and propose future studies that could improve our understanding of how chlamydial infertility in women occurs and possible future interventions to reduce this disease burden.

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“…Viable C. trachomatis can also persist in macrophages, and this may provide an alternative target cell for chlamydial replication in a number of infections; follicular fluid contains tissue macrophages in large amounts (14). Other authors suggested that in these patients the poor IVF outcome was associated with subclinical chlamydial infection (19)(20)(21)(22)(23)(24)(25)(26).…”

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confidence: 99%