NDLI: Microparticles from mycobacteria-infected macrophages promote inflammation and cellular migration.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Swain, Ashleigh Kieckbusch, Jens Latham, Sharissa L. Britton, Warwick J. Walters, Shaun B. Grau, Georges E. R. Combes, Valéry Saunders, Bernadette M. Nagalingam, Gayathri
Description	Country affiliation: Australia Author Affiliation: Walters SB ( Centenary Institute, Newtown, New South Wales 2042, Australia. b.saunders@centenary.org.au)
Abstract	Mycobacterium tuberculosis infection is characterized by a strong inflammatory response whereby a few infected macrophages within the granuloma induce sustained cellular accumulation. The mechanisms coordinating this response are poorly characterized. We hypothesized that microparticles (MPs), which are submicron, plasma membrane-derived vesicles released by cells under both physiological and pathological conditions, are involved in this process. Aerosol infection of mice with M. tuberculosis increased CD45(+) MPs in the blood after 4 wk of infection, and in vitro infection of human and murine macrophages with mycobacteria enhanced MP release. MPs derived from mycobacteria-infected macrophages were proinflammatory, and when injected into uninfected mice they induced significant neutrophil, macrophage, and dendritic cell recruitment to the injection site. When incubated with naive macrophages, these MPs enhanced proinflammatory cytokine and chemokine release, and they aided in the disruption of the integrity of a respiratory epithelial cell monolayer, providing a mechanism for the egress of cells to the site of M. tuberculosis infection in the lung. In addition, MPs colocalized with the endocytic recycling marker Rab11a within macrophages, and this association increased when the MPs were isolated from mycobacteria-infected cells. M. tuberculosis-derived MPs also carried mycobacterial Ag and were able to activate M. tuberculosis-specific CD4(+) T cells in vivo and in vitro in a dendritic cell-dependent manner. Collectively, these data identify an unrecognized role for MPs in host response against M. tuberculosis by promoting inflammation, intercellular communication, and cell migration.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	2
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-01-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Cell-derived Microparticles Immunology Macrophages Microbiology Mycobacterium Tuberculosis Tuberculosis Animals Antigens, Bacterial Biological Transport Cd4-positive T-lymphocytes Cell Communication Cell Line Cell Movement Metabolism Chemokines Biosynthesis Cytokines Dendritic Cells Endosomes Inflammation Mediators Leukocytes Lymphocyte Activation Mice Mice, Transgenic Rab Gtp-binding Proteins Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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