THE ROLE OF IMMUNE CELLS IN TRANSPORT OF CHLAMYDIA MURIDARUM FROM THE ILIAC LYMPH NODES TO THE SPLEEN AND THE GASTROINTESTINAL TRACT

Author

Besmir Hyseni, Southern Illinois University CarbondaleFollow

Date of Award

6-1-2021

Degree Name

Master of Science

Department

Molecular Biology Microbiology and Biochemistry

First Advisor

Konjufca, Vjollca

Abstract

Chlamydia trachomatis is the most common sexually transmitted bacterial pathogen worldwide. Chlamydia spp. infect epithelial cells of the respiratory, intestinal, and reproductive tracts. Chlamydial infections in women may lead to pelvic inflammatory disease, ectopic pregnancy, chronic pelvic pain, and infertility. In addition to infecting infection the female reproductive tract (FRT), Chlamydia also infects the gastrointestinal tract (GIT) of animals and humans. In mice Chlamydia muridarum disseminates from the FRT to the GIT via internal routes and in a stepwise manner. Initially Chlamydia spreads from the FRT to infect the FRT-draining iliac lymph nodes (ILNs), then the spleen, and then the GIT. The first step of this dissemination (FRT to ILN) is mediated by tissue CD11c+ DCs. Chlamydia transport from ILN to the spleen is dependent on cell transport and is mediated by sphingosine 1-phosphate (S1P) signaling. The third step of Chlamydia transport from the spleen to the GIT is significantly hindered in splenectomized mice. However, which cells mediate this transportation of the second and the third step remain unknown. Using mouse-specific C. muridarum as a model pathogen we show that following depletion of CD8+ T cells or monocytes, Chlamydia dissemination to the spleen and the GIT is significantly hindered. Furthermore, this study reveals that Chlamydia may infect various cell types which then mediate its dissemination internally. It remains to be determined what role systemic dissemination may have in Chlamydia pathogenesis.