Mycobacterium tuberculosis replicates within necrotic human macrophages.

Autor:	Lerner TR; Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London NW1 1AT, England, UK., Borel S; Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London NW1 1AT, England, UK., Greenwood DJ; Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London NW1 1AT, England, UK., Repnik U; Department of Biosciences, University of Oslo, 0371 Oslo, Norway., Russell MR; Electron Microscopy Science Technology Platform, The Francis Crick Institute, London NW1 1AT, England, UK., Herbst S; Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London NW1 1AT, England, UK., Jones ML; Electron Microscopy Science Technology Platform, The Francis Crick Institute, London NW1 1AT, England, UK., Collinson LM; Electron Microscopy Science Technology Platform, The Francis Crick Institute, London NW1 1AT, England, UK., Griffiths G; Department of Biosciences, University of Oslo, 0371 Oslo, Norway., Gutierrez MG; Host-Pathogen Interactions in Tuberculosis Laboratory, The Francis Crick Institute, London NW1 1AT, England, UK max.g@crick.ac.uk.
Jazyk:	angličtina
Zdroj:	The Journal of cell biology [J Cell Biol] 2017 Mar 06; Vol. 216 (3), pp. 583-594. Date of Electronic Publication: 2017 Feb 27.
DOI:	10.1083/jcb.201603040
Abstrakt:	Mycobacterium tuberculosis modulation of macrophage cell death is a well-documented phenomenon, but its role during bacterial replication is less characterized. In this study, we investigate the impact of plasma membrane (PM) integrity on bacterial replication in different functional populations of human primary macrophages. We discovered that IFN-γ enhanced bacterial replication in macrophage colony-stimulating factor-differentiated macrophages more than in granulocyte-macrophage colony-stimulating factor-differentiated macrophages. We show that permissiveness in the different populations of macrophages to bacterial growth is the result of a differential ability to preserve PM integrity. By combining live-cell imaging, correlative light electron microscopy, and single-cell analysis, we found that after infection, a population of macrophages became necrotic, providing a niche for M. tuberculosis replication before escaping into the extracellular milieu. Thus, in addition to bacterial dissemination, necrotic cells provide first a niche for bacterial replication. Our results are relevant to understanding the environment of M. tuberculosis replication in the host. (© 2017 Lerner et al.)
Databáze:	MEDLINE
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