Nadel J A
Section of Pulmonary Diseases, University of California, San Francisco 94143-0130.
Allergy Proc. 1991 Mar-Apr;12(2):85-8. doi: 10.2500/108854191779011774.
Neurogenic inflammation produces potent responses in multiple cells in the airways. These responses normally are limited by the presence on the surface of target cells of neutral endopeptidase (NEP), an enzyme that cleaves and inactivates neuropeptides that come in close contact with the cell and thereby limits neurogenic inflammatory responses. Inhibition of NEP by drugs, respiratory viruses, cigarette smoke, and toluene diisocyanate result in exaggerated neurogenic responses, while upregulation of NEP (e.g., by corticosteroids) may suppress the responses. Exogenously delivered recombinant human NEP also inhibits the responses. The novel system whereby sensory nerve stimulation results in the release of inflammatory neuropeptides provides a potentially important mechanism in the pathogenesis of airway inflammation. The strategies discussed here provide tools for the investigation of this system and suggests methods for therapeutic intervention.
神经源性炎症会在气道的多种细胞中引发强烈反应。这些反应通常受到靶细胞表面中性内肽酶（NEP）的限制，NEP是一种酶，它能切割并使与细胞紧密接触的神经肽失活，从而限制神经源性炎症反应。药物、呼吸道病毒、香烟烟雾和甲苯二异氰酸酯对NEP的抑制会导致过度的神经源性反应，而NEP的上调（例如通过皮质类固醇）可能会抑制这些反应。外源性递送的重组人NEP也能抑制这些反应。感觉神经刺激导致炎症性神经肽释放的新系统为气道炎症的发病机制提供了一个潜在的重要机制。这里讨论的策略为研究该系统提供了工具，并提出了治疗干预的方法。
