Tesfaye Belay1, Anthony Woart. 1. School of Arts and Sciences, Bluefield State College, Bluefield, WV, United States. Electronic address: tbelay@bluefieldstate.edu.
Abstract
BACKGROUND/PURPOSE(S): Genital infection by Chlamydia trachomatis (CT) is the most common bacterial sexually transmitted disease worldwide. The infection can cause serious reproductive health complications including pelvic inflammatory disease and infertility. Stress is implicated as a risk factor for various infections; however, its effect on Chlamydia genital infection and complications are unknown. METHODS: We investigated the effect of cold-stress on resistance to Chlamydia genital infection, stress hormone production, and the functions of immune cells in a mouse model. Mice were infected intravaginally with CT after a 24-day cold-stress application. The course of infection was monitored by cervicovaginal swabbing for isolation of live Chlamydia in tissue culture. The production of stress hormones and cytokines in genital tracts, spleen or blood were assessed. RESULTS: Exposure of mice to 24-day stress resulted in: (a) increased susceptibility to Chlamydia genital infection and greater intensity of infection, (b) increased plasma or tissue noradrenaline and adrenaline levels, and (c) decreased mRNA and protein levels of major cytokines and chemokines in the spleen and genital tract. CONCLUSION: These results suggest that cold-induced stress induces the production of catecholamines, which may play a critical role in the modulation of the immune system leading to increased susceptibility and greater intensity of Chlamydia genital infection that could promote the development of complications.
BACKGROUND/PURPOSE(S): Genital infection by Chlamydia trachomatis (CT) is the most common bacterial sexually transmitted disease worldwide. The infection can cause serious reproductive health complications including pelvic inflammatory disease and infertility. Stress is implicated as a risk factor for various infections; however, its effect on Chlamydia genital infection and complications are unknown. METHODS: We investigated the effect of cold-stress on resistance to Chlamydia genital infection, stress hormone production, and the functions of immune cells in a mouse model. Mice were infected intravaginally with CT after a 24-day cold-stress application. The course of infection was monitored by cervicovaginal swabbing for isolation of live Chlamydia in tissue culture. The production of stress hormones and cytokines in genital tracts, spleen or blood were assessed. RESULTS: Exposure of mice to 24-day stress resulted in: (a) increased susceptibility to Chlamydia genital infection and greater intensity of infection, (b) increased plasma or tissue noradrenaline and adrenaline levels, and (c) decreased mRNA and protein levels of major cytokines and chemokines in the spleen and genital tract. CONCLUSION: These results suggest that cold-induced stress induces the production of catecholamines, which may play a critical role in the modulation of the immune system leading to increased susceptibility and greater intensity of Chlamydia genital infection that could promote the development of complications.