Journal article

Mycobacterium tuberculosis: Rewiring host cell signaling to promote infection

MD Stutz, MP Clark, M Doerflinger, M Pellegrini

Journal of Leukocyte Biology | WILEY | Published : 2018

Abstract

The ability of Mycobacterium tuberculosis to cause disease hinges upon successfully thwarting the innate defenses of the macrophage host cell. The pathogen's trump card is its armory of virulence factors that throw normal host cell signaling into disarray. This process of subverting the macrophage begins upon entry into the cell, when M. tuberculosis actively inhibits the fusion of the bacilli-laden phagosomes with lysosomes. The pathogen then modulates an array of host signal transduction pathways, which dampens the macrophage's host-protective cytokine response, while simultaneously adapting host cell metabolism to stimulate lipid body accumulation. Mycobacterium tuberculosis also renovate..

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University of Melbourne Researchers

Grants

Awarded by Sylvia and Charles Viertel Charitable Foundation


Funding Acknowledgements

This work was supported by the National Health and Medical Research Council Australia (Grants 1006592, 1045549, and 1065626 to M.P.), The Sylvia & Charles Viertel Senior Medical Research Fellowship (M.P.), the Victorian State Government Operational Infrastructure Support, and the Independent Research Institutes Infrastructure Support Scheme of the Australian Government National Health and Medical Research Council.