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© Biologie structurale et chimie
Structure du domaine en doigt de zinc de la protéine NEMO, déterminée par Résonance magnétique nucléaire (RMN). Cette protéine jouant un rôle dans des maladies (cancer, inflammation), les connaissances acquises sur sa structure offrent de précieuses informations sur sa fonction.
Publication : Elife

Intracellular growth of Mycobacterium tuberculosis after macrophage cell death leads to serial killing of host cells.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Elife - 28 Jan 2017

Mahamed D, Boulle M, Ganga Y, Mc Arthur C, Skroch S, Oom L, Catinas O, Pillay K, Naicker M, Rampersad S, Mathonsi C, Hunter J, Wong EB, Suleman M, Sreejit G, Pym AS, Lustig G, Sigal A

Link to Pubmed [PMID] – 28130921

Elife. 2017 May 5;6. pii: e28205

A hallmark of pulmonary tuberculosis is the formation of macrophage-rich granulomas. These may restrict Mycobacterium tuberculosis (Mtb) growth, or progress to central necrosis and cavitation, facilitating pathogen growth. To determine factors leading to Mtb proliferation and host cell death, we used live cell imaging to track Mtb infection outcomes in individual primary human macrophages. Internalization of Mtb aggregates caused macrophage death, and phagocytosis of large aggregates was more cytotoxic than multiple small aggregates containing similar numbers of bacilli. Macrophage death did not result in clearance of Mtb. Rather, it led to accelerated intracellular Mtb growth regardless of prior activation or macrophage type. In contrast, bacillary replication was controlled in live phagocytes. Mtb grew as a clump in dead cells, and macrophages which internalized dead infected cells were very likely to die themselves, leading to a cell death cascade. This demonstrates how pathogen virulence can be achieved through numbers and aggregation states.

https://www.ncbi.nlm.nih.gov/pubmed/?term=28130921