Nitric oxide and asthmatic inflammation.
Asthmatic patients show an increased expression of inducible nitric oxide synthase (iNOS) in airway epithelial cells and an increased level of nitric oxide (NO) in exhaled air. The NO derived from airway epithelial cells may be a mechanism for amplifying and perpetuating asthmatic inflammation, through inhibition of T helper 1 (Th1) cells and their production of interferon gamma (IFN-gamma). This would result in an increase in the number of Th2 cells and the cytokines interleukin 4 (IL-4) (which is important for IgE expression) and IL-5 (which plays a critical role in the recruitment of eosinophils into the airways). Although this mechanism may be part of our nonspecific airway defence against parasite invasion, it appears to have been activated inappropriately in asthma. Here, Peter Barnes and Eddy Liew argue that the development of specific iNOS inhibitors may represent a novel therapeutic approach for asthma and other allergic diseases.
Barnes
P J
PJ
Dept of Thoracic Medicine, National Heart and Lung Institute, London, UK.
Liew
F Y
FY
D000594:Amino Acid Oxidoreductases / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D001249:Asthma / Q000201:enzymology / Q000276:immunology* / Q000628:therapy; D006801:Humans; D009569:Nitric Oxide / Q000276:immunology*; D019001:Nitric Oxide Synthase
D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D000594:Amino Acid Oxidoreductases