Neville Berkman1, Annette Robichaud1, Richard Robbins1, G. Roesems1, E.-B. Haddad1, Peter J. Barnes1, Kian Fan Chung1
1Department of Thoracic Medicine, National HeartLung Institute, Imperial College of Science, TechnologyMedicine, London, UK
Tóm tắt
Nitric oxide produced by the inducible enzyme, nitric oxide synthase (iNOS), is implicated in immunological and inflammatory processes. We determined the effects of T‐helper (Th)2‐derived cytokines on the induction of iNOS from an epithelial A549 cell line and human airway epithelial cells stimulated by a mixture of interleukin‐1β (IL‐1β), interferon‐γ (IFN‐γ) and tumour necrosis factor‐α (TNF‐α). Interleukin‐4 (IL‐4) and interleukin‐13 (IL‐13) but not interleukin‐10 (IL‐10) inhibited both iNOS mRNA expression and nitrite release in A549 cells. On human airway epithelial cells, IL‐4 and IL‐13 reduced iNOS mRNA expression. Dexamethasone also inhibited both iNOS expression and nitrite release. Th2 cytokines, IL‐4 and IL‐13, inhibit iNOS upregulation by Th1 cytokines, indicating an important reciprocal role of Th1 and Th2 T‐cell subsets on lung epithelial cells.
