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Escape of Mycobacterium tuberculosis from oxidative killing by neutrophils.

Journal article
Authors Björn Corleis
Daniel Korbel
Robert Wilson
Johan Bylund
Ronnie Chee
Ulrich E Schaible
Published in Cellular microbiology
Volume 14
Issue 7
Pages 1109-1121
ISSN 1462-5822
Publication year 2012
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Pages 1109-1121
Language en
Subject categories Clinical Medicine


Neutrophils enter sites of infection, where they can eliminate pathogenic bacteria in an oxidative manner. Despite their predominance in active tuberculosis lesions, the function of neutrophils in this important human infection is still highly controversial. We observed that virulent Mycobacterium tuberculosis survived inside human neutrophils despite prompt activation of these defence cells' microbicidal effectors. Survival of M. tuberculosis was accompanied by necrotic cell death of infected neutrophils. Necrotic cell death entirely depended on radical oxygen species production since chronic granulomatous disease neutrophils were protected from M. tuberculosis-triggered necrosis. More, importantly, the M.  tuberculosisΔRD1 mutant failed to induce neutrophil necrosis rendering this strain susceptible to radical oxygen species-mediated killing. We conclude that this virulence function is instrumental for M. tuberculosis to escape killing by neutrophils and contributes to pathogenesis in tuberculosis.

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