Immune Regulation of Chlamydia trachomatis Infections of the Female Genital Tract

Abstract

Tubal infertility and reproductive damage, preeclampsia and preterm births may potentially occur in many of the 50 million women who are annually infected with Chlamydia trachomatis [reviewed in 1; 2- 4]. C.trachomatis infections of the genital tract are also reported to increase the risk of human immunodeficiency virus type 1(HIV-1) susceptibility and viral shedding in the genital tract either directly by pro-inflammatory signalling pathways or indirectly by their effects on genital epithelial cells [5]. A dramatic increase in the number of HIV-1 chemokine co-receptor CXCR4- and CCR5-positive T cell targets has also been reported in the endocervix of C. trachomatis-positive women [6]. Gynecological cancer development is also suggested to be linked with Chlamydial genital tract infections. Epidemiological reports have proposed that C.trachomatis may act as a co-factor in the development of human papilloma virus (HPV)-induced squamous cell carcinomas (SCC), with an association between distinct serovariants of C. trachomatis (B, D, E, G, I, and J) and SCC being reported [7,8]. It is also likely that C. trachomatis co-infections of the lower genital tract (LGT) play a role in carcinogenesis of the female upper genital tract (UGT), particularly epithelial ovarian and type II carcinomas [9,10]. To explain the epidemiological associations of Chlamydial infections cervical and ovarian cancer development it has been hypothesised that the pathogen perhaps triggers epigenetic changes in host chromatin and impairs host DNA repair pathways [11] or that it changes host cell survival pathways by disrupting DNA damage signalling pathways associated with tumorigenesis [12]...