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© Research
Publication : Cell reports

Mycobacterium tuberculosis Controls Phagosomal Acidification by Targeting CISH-Mediated Signaling

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Cell reports - 26 Sep 2017

Queval CJ, Song OR, Carralot JP, Saliou JM, Bongiovanni A, Deloison G, Deboosère N, Jouny S, Iantomasi R, Delorme V, Debrie AS, Park SJ, Gouveia JC, Tomavo S, Brosch R, Yoshimura A, Yeramian E, Brodin P

Link to Pubmed [PMID] – 28954234

Cell Rep 2017 Sep;20(13):3188-3198

Pathogens have evolved a range of mechanisms to counteract host defenses, notably to survive harsh acidic conditions in phagosomes. In the case of Mycobacterium tuberculosis, it has been shown that regulation of phagosome acidification could be achieved by interfering with the retention of the V-ATPase complexes at the vacuole. Here, we present evidence that M. tuberculosis resorts to yet another strategy to control phagosomal acidification, interfering with host suppressor of cytokine signaling (SOCS) protein functions. More precisely, we show that infection of macrophages with M. tuberculosis leads to granulocyte-macrophage colony-stimulating factor (GM-CSF) secretion, inducing STAT5-mediated expression of cytokine-inducible SH2-containing protein (CISH), which selectively targets the V-ATPase catalytic subunit A for ubiquitination and degradation by the proteasome. Consistently, we show that inhibition of CISH expression leads to reduced replication of M. tuberculosis in macrophages. Our findings further broaden the molecular understanding of mechanisms deployed by bacteria to survive.

https://www.ncbi.nlm.nih.gov/pubmed/28954234