Inhibition of Respiration by Nitric Oxide Induces a Mycobacterium tuberculosis Dormancy Program
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ABSTRACT: An estimated two billion persons are latently infected with Mycobacterium tuberculosis. The host factors that initiate and maintain this latent state and the mechanisms by which M. tuberculosis survives within latent lesions are compelling but unanswered questions. One such host factor may be nitric oxide (NO), a product of activated macrophages that exhibits antimycobacterial properties. Evidence for the possible significance of NO comes from murine models of tuberculosis showing progressive infection in animals unable to produce the inducible isoform of NO synthase and in animals treated with a NO synthase inhibitor. Here, we show that O2 and low, nontoxic concentrations of NO competitively modulate the expression of a 48-gene regulon, which is expressed in vivo and prepares bacilli for
ORGANISM(S): Mycobacterium tuberculosis
SUBMITTER: SMD Staff
PROVIDER: E-GEOD-8839 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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