Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.

Sci. STKE, 2 July 2002
Vol. 2002, Issue 139, p. tw236
[DOI: 10.1126/stke.2002.139.tw236]


Immunology Infection Protection During Inflammation

During microbial infection, neutrophils generate microbicidal agents through the release of myeloperoxidase (MPO). Eiserich et al. report that MPO's actions during inflammation extend beyond generating antimicrobial oxidizing species. MPO permeates the mammalian vasculature and alters blood vessel function during acute inflammation by catabolizing nitric oxide (NO). NO is an endothelial-derived blood vessel relaxant that is produced in response to endotoxin. By reducing NO availability, MPO impairs vascular changes produced by infection. This finding may explain the increased susceptibility of humans deficient in MPO to infection.

J. P. Eiserich, S. Baldus, M.-L. Brennan, W. Ma, C. Zhang, A. Tousson, L. Castro, A. J. Lusis, W. M. Nauseef, C. R. White, B. A. Freeman, Myeloperoxidase, a leukocyte-derived vascular NO oxidase. Science 296, 2391-2394 (2002). [Abstract] [Full Text]

Citation: Infection Protection During Inflammation. Sci. STKE 2002, tw236 (2002).

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882