[Arginine metabolism in bronchial asthma].

Asthma is a chronic inflammatory disorder of the airways in which many cells and cellular elements play a role. Airway inflammation is associated with an enhanced expression of inducible nitric oxide synthase. This increases nitric oxide production and results in higher levels of NO* gas in exhaled air. Measurement of exhaled nitric oxide is a very useful non-invasive method in the diagnosis and treatment monitoring of asthma. However, the role of nitric oxide in asthma, still under intense debate, should not be regarded only as a consequence of its abundance, but rather as an impairment of the mechanisms that regulate its synthesis and activity, including reducing nitric oxide production by neuronal and endothelial synthase. Arginine is a substrate for both nitric oxide synthase and arginase. Arginase expression in the lung is strongly induced by cytokines, in particular IL-4 and IL-13, which are produced at elevated level in asthmatic airways and which activate inflammatory pathways. Arginase modulates nitric oxide synthase activity and provides a precursor for polyamines (putrescine, spermidine, and spermine) and proline, which stimulate cell growth and collagen synthesis, respectively. Therefore, arginase might also be involved in inflammation-induced airway remodeling in chronic asthma. This review presents arginine homeostasis in asthma and focuses not only on inducible nitric oxide synthase, but also on impairment of constitutive nitric oxide synthase activity and the overproduction of arginase downstream products.