Inactivation of <Emphasis Type="Italic">Burkholderia pseudomallei</Emphasis><Emphasis Type="Italic">bsaQ</Emphasis> results in decreased invasion efficiency and delayed escape of bacteria from endocytic vesicles |
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Authors: | Veerachat Muangsombut Supaporn Suparak Pornpan Pumirat Suwat Damnin Paiboon Vattanaviboon Visith Thongboonkerd Sunee Korbsrisate |
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Institution: | (1) Department of Immunology, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, 10700, Thailand;(2) Laboratory of Biotechnology, Chulabhorn Research Institute, Chulabhorn Graduate Institute, Lak Si, Bangkok, 10210, Thailand;(3) Medical Proteomics Unit and Medical Molecular Biology Unit, Office for Research and Development, Faculty of Medicine Siriraj Hospital, Mahidol University, Bangkok, 10700, Thailand |
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Abstract: | 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.
Veerachat Muangsombut and Supaporn Suparak contributed equally to this work. |
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Keywords: | Burhkolderia pseudomallei Type III secretion system BsaQ Invasion Escaping endocytic vesicles Multinucleated giant cell |
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