What is the role of toll-like receptor (TLR) in the induction of tubal damages caused by chlamydia trachomatis infection?

Abstract

Introduction: the susceptibility, course, complications and outcome of Chlamydia trachomatis infection depends on the type of bacteria, environmental factors and host genetic factors. Among women, the most common infection is cervicitis that can be complicated by salpingitis leading to tubal damage. It is believed that long-term complications occur via HSP 60 and toll-like receptors. Objective: to conduct a systematic review of published articles that studied tubal alterations caused by Chlamydia trachomatis infection and the role of toll like receptors during this process. Methods: to perform this review, three reviewers conducted extensive research in major scientific databases: PubMed, Lilacs, Embase, Cochrane library, Google Schoolar and Highwire. The keywords used were: Chlamydia or Chlamydia trachomatis and Chlamydia infections or toll like receptors and toll-like receptor or receptor, toll-like diseases fallopian tube occlusion or tubal obstruction or tubal. Studies in English, Portuguese and Spanish were included. Studies excluded: literature review, studies published in other languages and studies without experimental design set. The evaluation was performed as recommended by the Brazilian Medical Association (from 2000 to 2012). Results: we found 536 articles, of which 11 were included in this study. After a qualitative assessment, we selected six articles. In our research we found that TLR2 knockout mice were associated with tubal pathology protection. Another experimental model using mice, demonstrate that IFN-beta and IP-10 activation during C. trachomatis infection are not TRL2 and TLR4 dependent, but MyD88 dependent. An integration between a clinical and an experimental model showed that TLR4 is associated to severity but not to susceptibility to C. trachomatis infection. In women it was observed increased expressions in TLR4 and NFκB in the tubal epithelium, indicating a possible involvement in the increased PROKR-2, which predisposes to ectopic pregnancy. Another study showed that the presence of SNPs in multiple genes doubled the risk of tubal pathology in C. trachomatis infected women. Finally, it is believed that genetic variations in the immune system might have an impact in the susceptibility and severity to the genital infection by C. trachomatis. Conclusion: these studies showed a minor involvement of TLR4 in the pathogenesis of tubal damage induced by C. trachomatis, while TLR2 have a major role in this process and it is dependent of the immune system genetic variations.