Nitric oxide synthase inhibitors attenuate ozone-induced airway inflammation in guinea pigs: possible role of interleukin-8

Inoue, H; Aizawa, H; Nakano, H; Matsumoto, K; Kuwano, K; Nadel, JA; Hara, N

HERO ID

12005

Reference Type

Journal Article

Year

2000

Language

English

PMID

10619828

HERO ID 12005
In Press No
Year 2000
Title Nitric oxide synthase inhibitors attenuate ozone-induced airway inflammation in guinea pigs: possible role of interleukin-8
Authors Inoue, H; Aizawa, H; Nakano, H; Matsumoto, K; Kuwano, K; Nadel, JA; Hara, N
Journal American Journal of Respiratory and Critical Care Medicine
Volume 161
Issue 1
Page Numbers 249-256
Abstract Nitric oxide (NO) is increased in exhaled air of asthmatics. We hypothesized that endogenous NO contributes to airway inflammation and hyperresponsiveness, and that interleukin-8 (IL-8) might be involved in this mechanism. In human transformed bronchial epithelial cells in vitro, NO donors increased IL-8 production dose-dependently. In addition, tumor necrosis factor-"alpha" (TNF-"alpha") plus IL-1"beta" plus interferon-"gamma" (IFN-"gamma") increased IL-8 in culture supernatant of epithelial cells; the combination of NO synthase (NOS) inhibitors, aminoguanidine (AG) plus NG-nitro-L-arginine methyl ester (L-NAME) attenuated the cytokine-induced IL-8 production in epithelial cells. In guinea pigs in vivo, ozone exposure induced airway hyperresponsiveness to acetylcholine and increased neutrophils in bronchoalveolar lavage fluid (BALF), and these changes persisted for at least 5 h. Pretreatment with NOS inhibitors had no effect on airway hyperresponsiveness or neutrophil accumulation immediately after ozone, but significantly inhibited the changes 5 h after ozone. NOS inhibitors also attenuated the increases of nitrite/nitrate levels in BALF and the IL-8 mRNA expression in epithelial cells and in neutrophils in guinea pig airways 5 h after ozone. These results suggest that endogenous NO may play an important role in the persistent airway inflammation and hyperresponsiveness after ozone exposure, presumably partly through the upregulation of IL-8.
Doi 10.1164/ajrccm.161.1.9804096
Pmid 10619828
Wosid WOS:000084820200041
Is Certified Translation No
Dupe Override No
Comments ECRIB.Am. J. Respir. Crit. Care Med. 161: 249-256.
Is Public Yes
Language Text English
Is Qa No