Modulation of Immune Response by Epithelial cells During Chlamydia trachomatis Infection

Abstract

Chlamydia trachomatis infects epithelial cells at mucosal surfaces, and are the major causes of sexually transmitted diseases. In women, C. trachomatis infection can lead to complications, including pelvic inflammatory disease (PID) and its subsequent sequelae, including ectopic pregnancy and infertility. Infection is characterized by inflammation which is exacerbated upon reinfection, ultimately leading to tissue damage and scarring. Epithelial cells in the genital tract constitute a physical barrier and the first line of host defence that C. trachomatis encounters. The mechanism that modulate host responses to C. trachomatis infection have not been well defined largely due to asymptomatic nature of the disease it causes and incomplete understanding of its natural history. newlineThus, in the present study host-pathogen immune responses in cervical lymphocytes and PBMCs obtained from Chlamydia positive and negative women attending the gynecology out-patient department of Safdarjung Hospital, New Delhi were assessed. newlineEx vivo cervical lymphocytes and PBMCs obtained from C. trachomatis +ve and ve women were stimulated with recombinant chlamydial major outer membrane protein (MOMP) antigen and lymphoproliferative responses and secreted cytokines were evaluated. Median proliferative responses were found significantly higher in cervical lymphocytes compared to PBMCs. The chlamydial MOMP induced significantly high levels of secreted cytokines IL-6 and IL-10 and lower interferon-gamma (IFN-g) in cervical lymphocytes of Chlamydia positive women, indicating a T helper 2 response. On stimulation of PBMC obtained from Chlamydia-positive women, the median levels of IL-10, IL-12 and IFN-g were higher than in controls, but the differences were not significant. Our in vitro study suggests that the mucosal immune responses in Chlamydia trachomatis infection different from those newlineof PBMCs and are more helpful in understanding the cytokine responses in the female genital tract during chlamydial infection.