Chlamydia trachomatis perturb antigen cross presentation by Rab14 transport alteration on infect dendritic cells.

DEL BALZO D; CAPMANY A; CEBRIAN I; DAMIANI MT

Parana

Congreso; LIV Reunión Anual de la Sociedad Argentina de Investigación en Bioquímica y Biología Molecular; 2018

Sociedad Argentina de Investigación en Bioquímica y Biología Molecular

Chlamydia trachomatis is an obligate intracellular bacterium that replicates inside a vesicle called inclusion and is the most common sexually transmitted bacterial. This pathogen manipulates Rab GTPases, master controllers of vesicular transport, to ensure its survival and replication. Dendritic cells (DC) are the most powerful antigen presenting cells of the immune system and there are an essential link between innate and adaptive immunity. We have shown that Chlamydia trachomatis intercepts Rab14-vesicles to acquire host lipids necessary for its growth and multiplication. Furthermore, it is known that conventional DC requires Insulin-regulated aminopeptidase (IRAP)-Rab14 endosomes for efficient cross-presentation. Our hypothesis is that C. trachomatis recruits Rab14 not only as a strategy for nourishment, but also to interfere with the process of antigen presentation. By confocal microscopy, we observed that Rab14 is associated with the plasma membrane at the entry site of the bacterium. Later, Rab14 is recruited to the chlamydial inclusions and remains throughout the entire cycle. Interestingly, there are two populations of chlamidial inclusions, one small and not developed that colocalize with EEA1 or LAMP1 and another big and developed that recruit Rab14 and scape from degradative pathway. The knockdown of Rab14 causes a redistribution of MHC-I molecules and interferes with their transport towards the plasma membrane, assessed by flow cytometry. Additionally, it should also be noted that the infection does not alter the CMH-I expression, demonstrated by western blot assay.