NDLI: Bacterial Membrane Vesicles Mediate the Release of Mycobacterium tuberculosis Lipoglycans and Lipoproteins from Infected Macrophages.

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Bacterial Membrane Vesicles Mediate the Release of Mycobacterium tuberculosis Lipoglycans and Lipoproteins from Infected Macrophages.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wang, Ying McDonald, David J. Wearsch, Pamela A. Harding, Clifford V. Athman, Jaffre J. Boom, W. Henry
Description	Author Affiliation: Athman JJ ( Department of Pathology, Case Western Reserve University/University Hospitals Case Medical Center, Cleveland, OH); Wang Y ( Department of Pathology, Case Western Reserve University/University Hospitals Case Medical Center, Cleveland, OH); McDonald DJ ( Department of Molecular Biology and Microbiology, Case Western Reserve University/University Hospitals Case Medical Center, Cleveland, OH); Boom WH ( Center for AIDS Research, Case Western Reserve University/University Hospitals Case Medical Center, Cleveland, OH); Harding CV ( Department of Pathology, Case Western Reserve University/University Hospitals Case Medical Center, Cleveland, OH); Wearsch PA ( Department of Pathology, Case Western Reserve University/University Hospitals Case Medical Center, Cleveland, OH)
Abstract	Mycobacterium tuberculosis is an intracellular pathogen that infects lung macrophages and releases microbial factors that regulate host defense. M. tuberculosis lipoproteins and lipoglycans block phagosome maturation, inhibit class II MHC Ag presentation, and modulate TLR2-dependent cytokine production, but the mechanisms for their release during infection are poorly defined. Furthermore, these molecules are thought to be incorporated into host membranes and released from infected macrophages within exosomes, 40-150-nm extracellular vesicles that derive from multivesicular endosomes. However, our studies revealed that extracellular vesicles released from infected macrophages include two distinct, largely nonoverlapping populations: one containing host cell markers of exosomes (CD9, CD63) and the other containing M. tuberculosis molecules (lipoglycans, lipoproteins). These vesicle populations are similar in size but have distinct densities, as determined by separation on sucrose gradients. Release of lipoglycans and lipoproteins from infected macrophages was dependent on bacterial viability, implicating active bacterial mechanisms in their secretion. Consistent with recent reports of extracellular vesicle production by bacteria (including M. tuberculosis), we propose that bacterial membrane vesicles are secreted by M. tuberculosis within infected macrophages and subsequently are released into the extracellular environment. Furthermore, extracellular vesicles released from M. tuberculosis-infected cells activate TLR2 and induce cytokine responses by uninfected macrophages. We demonstrate that these activities derive from the bacterial membrane vesicles rather than exosomes. Our findings suggest that bacterial membrane vesicles are the primary means by which M. tuberculosis exports lipoglycans and lipoproteins to impair effector functions of infected macrophages and circulate bacterial components beyond the site of infection to regulate immune responses by uninfected cells.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1402894
Journal	The Journal of Immunology
Issue Number	3
Volume Number	195
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2015-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Exosomes Metabolism Macrophages, Alveolar Immunology Mycobacterium Tuberculosis Secretory Vesicles Tuberculosis, Pulmonary Animals Cells, Cultured Lipopolysaccharides Lipoproteins Lung Cytology Microbiology Mice Mice, Inbred C57bl Toll-like Receptor 2 Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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