The Burkholderia pseudomallei type III secretion system and BopA are required for evasion of LC3-associated phagocytosis.

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 an...

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Autores principales:	Lan Gong, Meabh Cullinane, Puthayalai Treerat, Georg Ramm, Mark Prescott, Ben Adler, John D Boyce, Rodney J Devenish
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/354c2999ea0c40f682bc5c107c999e03
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spelling	oai:doaj.org-article:354c2999ea0c40f682bc5c107c999e032021-11-18T06:57:23ZThe Burkholderia pseudomallei type III secretion system and BopA are required for evasion of LC3-associated phagocytosis.1932-620310.1371/journal.pone.0017852https://doaj.org/article/354c2999ea0c40f682bc5c107c999e032011-03-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21412437/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203Burkholderia 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 in single-membrane phagosomes rather than double-membrane autophagosomes, suggesting that LC3 is recruited to B. pseudomallei-containing phagosomes. Partial or complete loss of function of type III secretion system cluster 3 (TTSS3) in mutants lacking the BopA (effector) or BipD (translocator) proteins respectively, resulted in delayed or no escape from phagosomes. Consistent with these observations, bopA and bipD mutants both showed a higher level of co-localization with LC3 and the lysosomal marker LAMP1, and impaired survival in RAW264.7 cells, suggesting enhanced killing in phagolysosomes. We conclude that LC3 recruitment to phagosomes stimulates killing of B. pseudomallei trapped in phagosomes. Furthermore, BopA plays an important role in efficient escape of B. pseudomallei from phagosomes.Lan GongMeabh CullinanePuthayalai TreeratGeorg RammMark PrescottBen AdlerJohn D BoyceRodney J DevenishPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 3, p e17852 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Lan Gong Meabh Cullinane Puthayalai Treerat Georg Ramm Mark Prescott Ben Adler John D Boyce Rodney J Devenish The Burkholderia pseudomallei type III secretion system and BopA are required for evasion of LC3-associated phagocytosis.
description	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 in single-membrane phagosomes rather than double-membrane autophagosomes, suggesting that LC3 is recruited to B. pseudomallei-containing phagosomes. Partial or complete loss of function of type III secretion system cluster 3 (TTSS3) in mutants lacking the BopA (effector) or BipD (translocator) proteins respectively, resulted in delayed or no escape from phagosomes. Consistent with these observations, bopA and bipD mutants both showed a higher level of co-localization with LC3 and the lysosomal marker LAMP1, and impaired survival in RAW264.7 cells, suggesting enhanced killing in phagolysosomes. We conclude that LC3 recruitment to phagosomes stimulates killing of B. pseudomallei trapped in phagosomes. Furthermore, BopA plays an important role in efficient escape of B. pseudomallei from phagosomes.
format	article
author	Lan Gong Meabh Cullinane Puthayalai Treerat Georg Ramm Mark Prescott Ben Adler John D Boyce Rodney J Devenish
author_facet	Lan Gong Meabh Cullinane Puthayalai Treerat Georg Ramm Mark Prescott Ben Adler John D Boyce Rodney J Devenish
author_sort	Lan Gong
title	The Burkholderia pseudomallei type III secretion system and BopA are required for evasion of LC3-associated phagocytosis.
title_short	The Burkholderia pseudomallei type III secretion system and BopA are required for evasion of LC3-associated phagocytosis.
title_full	The Burkholderia pseudomallei type III secretion system and BopA are required for evasion of LC3-associated phagocytosis.
title_fullStr	The Burkholderia pseudomallei type III secretion system and BopA are required for evasion of LC3-associated phagocytosis.
title_full_unstemmed	The Burkholderia pseudomallei type III secretion system and BopA are required for evasion of LC3-associated phagocytosis.
title_sort	burkholderia pseudomallei type iii secretion system and bopa are required for evasion of lc3-associated phagocytosis.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/354c2999ea0c40f682bc5c107c999e03
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The Burkholderia pseudomallei type III secretion system and BopA are required for evasion of LC3-associated phagocytosis.

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