Authors: Korhonen, R.1; Lahti, A.1; Kankaanranta, H.1; Moilanen, E.1
Source: Current Drug Targets - Inflammation & Allergy, Volume 4, Number 4, August 2005 , pp. 471-479(9)
Publisher: Bentham Science Publishers
Abstract:
Nitric oxide (NO) is recognized as a mediator and regulator of inflammatory responses. It possesses cytotoxic properties that are aimed against pathogenic microbes, but it can also have damaging effects on host tissues. NO reacts with soluble guanylate cyclase to form cyclic guanosine monophosphate (cGMP), which mediates many of the effects of NO. NO can also interact with molecular oxygen and superoxide anion to produce reactive nitrogen species that can modify various cellular functions. These indirect effects of NO have a significant role in inflammation, where NO is produced in high amounts by inducible nitric oxide synthase (iNOS) and reactive oxygen species are synthesized by activated inflammatory cells. The present review deals with NO production and signaling in inflammation, especially in relation to human neutrophils and eosinophils.Keywords: drug development; macrophages; inflammatory mediators; nitric oxide synthase; inos expression; transcription; nitrosylation; ap pathway; jak-stat pathway
Document Type: Review article
Affiliations: 1: Immunopharmacology Research Group, Medical School, FIN-33014 University of Tampere, Finland.
Links for this article