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Am. J. Respir. Cell Mol. Biol., Volume 25, Number 5, November, 2001 606-612

What is the Role of Nitric Oxide in Murine and Human Host Defense against Tuberculosis?
Current Knowledge

Edward D. Chan, John Chan, and Neil W. Schluger

Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences Center and Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado; Department of Medicine, Albert Einstein School of Medicine, Bronx, New York; and Division of Pulmonary and Critical Care Medicine, Columbia University College of Physicians and Surgeons, New York, New York

The production of reactive oxygen intermediates and reactive nitrogen intermediates by innate immune cells is considered to be an effective host-defense mechanism against microbial pathogens. In the murine model of tuberculosis (TB), nitric oxide (NO) plays an essential role in the killing of Mycobacterium tuberculosis by mononuclear phagocytes. For example, in the mouse strain with a genetic disruption for inducible NO synthase (iNOS-/-), infection with M. tuberculosis is associated with a significantly higher risk of dissemination and mortality. Although more controversial in humans, there is a growing body of evidence that NO produced by TB-infected macrophages and by epithelial cells also has antimycobacterial effects against M. tuberculosis. The precise mechanism(s) by which NO and other reactive nitrogen species antagonize M. tuberculosis is not known, but may involve disruption of bacterial DNA, proteins, signaling, and/or induction of apoptosis of macrophages that harbor mycobacteria. In addition to cytokines such as tumor necrosis factor-alpha and interleukin 1-beta , mycobacterial cell wall components such as lipoarabinomannan and 19 kD lipoprotein, along with the T-cell-derived interferon-gamma , may also induce NO expression. In a Darwinian fashion, it also appears that certain strains of M. tuberculosis have evolved strategies to combat the toxic effects of NO.

Abbreviations: dendritic cells, DC; interferon, IFN; interleukin, IL; inducible nitric oxide synthase, iNOS; lipomannan, LAM; mannose-capped lipoarabinomannan, ManLAM; nitric oxide, NO; nitrogen dioxide, NO2; superoxide anion, O2-; peroxynitrite anion, ONOO-; dimannosylphosphatidylinositides, PIM2; reactive nitrogen intermediates, RNI; reactive oxygen intermediates, ROI; tuberculosis, TB; tumor necrosis factor, TNF.




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