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CUTTING EDGE |
*
Department of Microbiology and Immunology, The Howard Hughes Medical Institute, and
Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461; and
Glaxo Institute of Applied Pharmacology, University of Cambridge, Cambridge, United Kingdom
Signaling by extracellular nucleotides through P2 purinergic
receptors affects diverse macrophage functions; however, its role in
regulating antimicrobial radicals during bacterial infection has not
been investigated. Mycobacterium tuberculosis-infected
macrophages released ATP in a dose-dependent manner, which correlated
with nitrite accumulation. P2 receptor inhibitors, including oxidized
ATP, blocked NO synthase (NOSII) up-regulation and NO production
induced by infection with M. tuberculosis or bacille
Calmette-Guérin, or treatment with LPS or TNF-
. Oxidized ATP
also inhibited oxygen radical production and activation of NF-
B and
AP-1 in response to infection and inhibited NO-dependent killing of
bacille Calmette-Guérin by macrophages. Experiments using
macrophages derived from P2X7 gene-disrupted mice ruled out
an essential role for P2X7 in NOSII regulation. These data
demonstrate that P2 receptors regulate macrophage activation in
response to bacteria and proinflammatory stimuli, and suggest that
extracellular nucleotides released from infected macrophages may
enhance production of oxygen radicals and NO at sites of
infection.
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