Host HDL biogenesis machinery is recruited to the inclusion of Chlamydia trachomatis-infected cells and regulates chlamydial growth.

摘要: Summary Chlamydia trachomatis is an obligate intracellular bacterial pathogen that the most common cause of sexually transmitted infections and etiological agent trachoma, leading preventable blindness. The organism infects epithelial cells genital tract eyelid resulting in a damaging inflammatory response. Chlamydia grows within vacuole termed inclusion, its growth depends on numerous host factors, including lipids. Although variety mechanisms are involved acquisition cell cholesterol glycosphingolipids by C. trachomatis, none previously documented pathways for lipid absolutely required growth. Here we demonstrate multiple components high-density lipoprotein (HDL) biogenesis machinery effluxers, ABCA1 CLA 1, their extracellular acceptor, apoA-1, recruited to inclusion C. trachomatis-infected cells. Furthermore, apoA-1 accumulates colocalizes with pools phosphatidylcholine. Knockdown ABCA1, which mediates cellular efflux phospholipids initiate formation HDL serum, prevents C. trachomatis infected HeLa In addition, drugs inhibit transport activities 1 also recruitment prevent chlamydial growth.These results strongly suggest co-opts system acquire lipids, such as phosphatidylcholine, necessary