NO is an important mediator of immune and inflammatory responses. NO is produced from L-arginine by three isoforms of nitric oxide synthase (NOS), neuronal (nNOS; NOS1), endothelial (eNOS; NOS3) and inducible (iNOS). Exhaled NO has been shown to be increased in asthma and has been put forward as a marker of airways inflammation. Moreover, increased production of NO and peroxynitrite may be responsible for the oxidative damage and fibrosis seen in interstitial lung diseases. The present review focuses on clinical and laboratory studies that are aimed at identifying the role of NO in the physiopathology of these disorders.
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