Host lipid acquisition and maintenance of the Chlamydia replicative niche

About This Grant

SUMMARY Chlamydia trachomatis is the leading cause of sexually transmitted infections of bacterial origin. No vaccine is available. Infections are often asymptomatic, leading to long-term damage of the reproductive organs and deleterious effects on women reproductive health ranging from pelvic inflammatory disease to infertility. The identification and characterization of essential Chlamydia specific factors is paramount to help in the design of effective therapeutics and/or vaccine, but the lag in Chlamydia genetics and the obligate intracellular nature of the pathogens have complicated this process. Here, we identified the first essential Chlamydia inclusion membrane protein. Based on the phenotypes of the corresponding mutant and the link to sphingolipid acquisition, we propose to test the hypothesis that a single Inc protein plays an essential role in preserving the integrity of the replicative niche by mediating the non-vesicular trafficking of sphingolipid to the inclusion and thereby contributes to pathogenesis. Our multidisciplinary approach will provide answers to fundamental biological questions regarding the role of host lipid acquisition in preserving the integrity of the Chlamydia replicative niche and cause disease. Additionally, our studies will reveal how a single Inc protein contribute to this process, thereby reinforcing the potential of these Chlamydia specific proteins as targets to design effective therapeutics and/or vaccines.