Killing of Mycobacterium tuberculosis by Neutrophils: A Nonoxidative Process

To determine the role of oxygen radicals in the killing of Mycobacterium tuberculosis by neutrophils, the effects of free-radical inhibitors and enzymes, catalase, superoxide dismutase, taurine, deferoxamine, and histidine were evaluated. Changes in the viability of M. tuberculosis were determined b...

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Published in:The Journal of infectious diseases Vol. 162; no. 3; pp. 700 - 704
Main Authors: Jones, Gerald S., Amirault, Harold J., Andersen, Burton R.
Format: Journal Article
Language:English
Published: Chicago, IL The University of Chicago Press 01-09-1990
University of Chicago Press
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Summary:To determine the role of oxygen radicals in the killing of Mycobacterium tuberculosis by neutrophils, the effects of free-radical inhibitors and enzymes, catalase, superoxide dismutase, taurine, deferoxamine, and histidine were evaluated. Changes in the viability of M. tuberculosis were determined by agar plate colony counts and a radiometric assay. No impairment in killing was seen with any of the inhibitors or enzymes. Patients with chronic granulomatous disease (CGD) have a defect in the NADPH oxidase pathway, causing their neutrophils to be unable to generate oxygen radicals . Ifthese radicals are involved in killing, thenCGD neutrophils should be less effective killers of M. tuberculosis than normal neutrophils. There was no evidence by either measure of M. tuberculosis viability that CGD neutrophils were less bactericidal than normal neutrophils. Killing by normal neutrophils was also effective in the absence of serum. These results lead to the conclusion that the mechanism by which M. tuberculosis is killed by neutrophils is independent of the oxygen metabolic burst.
Bibliography:Reprintsand correspondence: Dr. Burton R. Andersen, West Side VA Medical Center (MP 151), 820 S. Damen Ave., Chicago, IL 60612.
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ISSN:0022-1899
1537-6613
DOI:10.1093/infdis/162.3.700