During microbial infection, neutrophils generate microbicidal
agents through the release of myeloperoxidase (MPO). Eiserich
et al. (p.
2391) 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.
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