DNA damage contributes to transcriptional and immunological dysregulation of testicular cells during Chlamydia infection

Abstract

Causing approximately 127 million infections globally each year, sexually transmitted Chlamydia trachomatis is a major bacterial pathogen of the human reproductive tract. 1 C. trachomatis research has primarily focussed on women, and the links between these infections and pathology, especially infertility, are relatively well established.However, the role of C. trachomatis in development of male reproductive tract disease is poorly understood. C. trachomatis-infected men have been reported as having abnormal sperm, which may lead to infertility. [2][3][4][5] Abnormalities in sperm are likely due to errors and disruption in spermatogenesis. This process occurs in the testes, which are susceptible to chlamydial infection. 6 There are several specialized testicular cell types that are critical for spermatogenesis, including Leydig cells (responsible for the production of testosterone and other androgens), 7 spermatogenic cells (including spermatogonial stem cells from which all sperm arise) 8 and Sertoli cells (form the

Metabolic imprint of an intracellular pathogen drives histone hypermethylation and tunes the host transcriptional response to infection

“…The decrease in SAM levels was expected as Chlamydia highjack SAM (33). Consistent with low SAM levels, we observed that DNA was slightly hypomethylated late in infection, as previously reported (34). How can protein hypermethylation and DNA hypomethylation be reconciled?…”

In Vitro Modelling of Chlamydia trachomatis Infection in the Etiopathogenesis of Male Infertility and Reactive Arthritis

“…In recent years, a study employing a murine model has postulated the direct infection of the seminiferous tubule epithelium, formed by Sertoli cells, as an interesting pathophysiological mechanism for C. trachomatis-mediated male infertility, leading to compromised spermatogenesis with reduced sperm count, motility and altered morphology of mature spermatozoa (Bryan et al, 2021).…”