the burkholderia pseudomallei type iii secretion system and bopa are required for evasion of lc3-associated phagocytosis这种举办iii型分泌系统和bopa所需逃税lc3-associated吞噬作用.pdf

The Burkholderia pseudomallei Type III Secretion System and BopA Are Required for Evasion of LC3-Associated Phagocytosis 1,3 2¤ 2,3 1 1 2,3 Lan Gong , Meabh Cullinane , Puthayalai Treerat , Georg Ramm , Mark Prescott , Ben Adler , John D. Boyce2,3*, Rodney J. Devenish1,3* 1 Department of Biochemistry and Molecular Biology, Monash University, Melbourne, Victoria, Australia, 2 Department of Microbiology, Monash University, Melbourne, Victoria, Australia, 3 Australian Research Council Centre of Excellence in Structural and Functional Microbial Genomics, Monash University, Melbourne, Victoria, Australia Abstract Burkholderia pseudomallei is the causative agent of melioidosis, a fatal infectious disease endemic in tropical regions worldwide, and especially prevalent in southeast Asia and northern Australia. This intracellular pathogen can escape from phagosomes into the host cytoplasm, where it replicates and infects adjacent cells. We previously demonstrated that, in response to B. pseudomallei infection of macrophage cell line RAW 264.7, a subset of bacteria co-localized with the autophagy marker protein, microtubule-associated protein light chain 3 (LC3), implicating autophagy in host cell defence against infection. Recent reports have suggested that LC3 can be recruited to both phagosomes and autophagosomes, thereby raising questions regarding the identity of the LC3-positive compartments in which invading bacteria reside and the mechanism of the autophagic response to B. pseudomallei infection. Electron microscopy analysis of infected cells demonstrated that the invading bacteria were either free in the cytosol, or sequestered