Chlamydia trachomatis infection decreses the secreation of galectin-1 by hijacking Rab39a

AGUSTIN LUJAN; RABINOVICH GA; CROCI DO; GAMBARTE TUDELA J; DAMIANI MT

Villa General Belgrano, Córdoba

Simposio; 2nd Argetinean Symposium of Glycobiology; 2016

IBYME-Instituto Leloir-CIQUIBIC

Chlamydia trachomatis (Ct) is the most prevalent bacterial sexually transmitted disease worldwide. Ct causes a broad range of acute genital pathologies such as cervicitis and pelvic inflammatory disease in women, and urethritis and orchitis in men. Chronic infections are responsible for severe reproductive tissue damage and lead to female tubal obstruction and infertility. Ct is an obligate intracellular bacterium that survives and replicates inside a modified-phagosome called the inclusion. Ct avoids killing at the phagocytic pathway by hijacking Rab proteins, the master controllers of vesicular transport. At the same time, the alteration of Rab functioning allows Ct to acquire nutrients from the host cell. Our laboratory has demonstrated that Ct recruits Rab39a to intercept multivesicular bodies enriched in sphingomyelin and cholesterol. Our results show that Rab39a co-localizes with galectin-1 at multivesicular bodies in Ct-infected cells. Interestingly, Ct recruits galectin-1 which is retained within cells along infection. In consequence, the release of galectin-1 to the media decreases in infected cells. Likely, a reduced level of extracellular galectin-1 may cause an imbalance in the Th1/Th2 response that could explain the persistent chronic inflammation underlying Ct infection that leads to scarring and fibrosis of the reproductive tissues.