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Sci. Signal., 8 June 2010
Vol. 3, Issue 125, p. ra45
[DOI: 10.1126/scisignal.2000549]

RESEARCH ARTICLES

Editor's Summary

Feedback for Function
Neutrophils migrate to sites of infection, where they kill pathogens by processes such as phagocytosis and the release of reactive oxygen species. However, activated neutrophils can also result in tissue damage and inflammatory diseases in the host; thus, a better understanding of the mechanisms that regulate neutrophil activation could help in the development of therapies that could curb their destructive side effects. Chen et al. found that neutrophils responded to a range of infectious and inflammatory signals by releasing adenosine triphosphate (ATP). In addition to its role as a cellular energy source, ATP and its metabolites function as intercellular signaling molecules by stimulating purinergic receptors. The authors found that stimulation of formyl peptide receptors (FPRs) on neutrophils triggered the release, through pannexin-1 hemichannels, of ATP that signaled in an autocrine fashion through P2Y2 receptors. Moreover, this autocrine signal was required for neutrophil activation. In addition, mice deficient in P2Y2 receptors were less capable of clearing bacteria than were their wild-type counterparts. Together, these data suggest that feedback signaling by ATP released by neutrophils contributes to their activation.

Citation: Y. Chen, Y. Yao, Y. Sumi, A. Li, U. K. To, A. Elkhal, Y. Inoue, T. Woehrle, Q. Zhang, C. Hauser, W. G. Junger, Purinergic Signaling: A Fundamental Mechanism in Neutrophil Activation. Sci. Signal. 3, ra45 (2010).

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