Inactivation of Burkholderia pseudomallei bsaQ results in decreased invasion efficiency and delayed escape of bacteria from endocytic vesicles.
Burkholderia pseudomallei, an infectious Gram-negative bacterium, is the causative pathogen of melioidosis. In the present study, a B. pseudomallei strain with mutation in the bsaQ gene, encoding a structural component of the type III secretion system (T3SS), was constructed. This bsaQ mutation caused a marked decrease in secretion of BopE effector and BipD translocator proteins into culture supernatant. The B. pseudomallei bsaQ mutant also exhibited decreased efficiencies of plaque formation, invasion into non-phagocytic cells and multinucleated giant cell (MNGC) development in a J774A.1 macrophage cell line. Co-localization of the bacteria and lysosome-associated membrane glycoprotein-1 (LAMP-1) containing vesicles suggested that defects in MNGC formation may result from the delayed ability of this B. pseudomallei mutant to escape from the vacuoles of macrophages.
Muangsombut
Veerachat
V
Department of Immunology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok 10700, Thailand.
Suparak
Supaporn
S
Pumirat
Pornpan
P
Damnin
Suwat
S
Vattanaviboon
Paiboon
P
Thongboonkerd
Visith
V
Korbsrisate
Sunee
S
D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics* / Q000378:metabolism; D016957:Burkholderia pseudomallei / Q000235:genetics / Q000502:physiology*; D002459:Cell Fusion; D004847:Epithelial Cells / Q000378:metabolism; D005798:Genes, Bacterial; D015726:Giant Cells / Q000378:metabolism; D006367:HeLa Cells; D006801:Humans; D008264:Macrophages / Q000378:metabolism; D008554:Melioidosis / Q000382:microbiology; D051379:Mice; D009154:Mutation; D022161:Transport Vesicles / Q000378:metabolism / Q000382:microbiology*; D014617:Vacuoles / Q000378:metabolism
D001426:Bacterial Proteins