| Literature DB >> 15546957 |
Markus Munder1, Faustino Mollinedo, Jero Calafat, Javier Canchado, Cristina Gil-Lamaignere, José M Fuentes, Claudia Luckner, Gwendolyn Doschko, Germán Soler, Klaus Eichmann, Frank-Michael Müller, Anthony D Ho, Martin Goerner, Manuel Modolell.
Abstract
The balance of arginine metabolism via nitric oxide synthase (NOS) or arginase is an important determinant of the inflammatory response of murine macrophages and dendritic cells. Here we analyzed the expression of the isoform arginase I in human myeloid cells. Using healthy donors and patients with arginase I deficiency, we found that in human leukocytes arginase I is constitutively expressed only in granulocytes and is not modulated by a variety of proinflammatory and anti-inflammatory stimuli in vitro. We demonstrate that arginase I is localized in azurophil granules of neutrophils and constitutes a novel antimicrobial effector pathway, likely through arginine depletion in the phagolysosome. Our findings demonstrate important differences between murine and human leukocytes with respect to regulation and function of arginine metabolism via arginase.Entities:
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Year: 2004 PMID: 15546957 DOI: 10.1182/blood-2004-07-2521
Source DB: PubMed Journal: Blood ISSN: 0006-4971 Impact factor: 22.113