期刊
LUNG
卷 194, 期 1, 页码 121-124出版社
SPRINGER
DOI: 10.1007/s00408-015-9833-4
关键词
Nitric oxide; Nitric oxide synthase; Eosinophilic inflammation; Bronchial asthma
资金
- Ministry of Education, Science, Sports and Culture [24591183]
- Grants-in-Aid for Scientific Research [24591183, 15K09236, 26500022] Funding Source: KAKEN
Background Asthma is characterized by airflow limitation with chronic airway inflammation, hyperresponsiveness and mucus hypersecretion. NO is generated by three nitric oxide synthase (i/n/eNOSs) isoforms, but conflicting results have been reported using asthmatic mice treated with NOSs inhibitors and NOS-knockout mice. To elucidate the authentic role of NO/NOSs in asthma, we used asthmatic mice lacking all NOSs (n/i/eNOS(-/-)). MethodsWild-type and n/i/eNOS(-/-) mice were sensitized and challenged with ovalbumin. Pathological findings and expressions of interferon (IFN)-gamma, interleukin (IL)-4, -5, -10, -13 and chemokines in the lung were evaluated. ResultsDecreased eosinophilic inflammation, bronchial thickening and mucus secretion, IL-4, -5 and -13, monocyte chemoattractant protein-1, eotaxin-1 and thymus and activation-regulated chemokine expressions were observed in n/i/eNOS(-/-) mice compared to wild-type, but expressions of IFN-gamma and IL-10 were similar. ConclusionUsing asthmatic n/i/eNOS(-/-) mice, NO plays important roles in accelerating bronchial eosinophilic inflammation and mucus hypersecretion in the pathophysiology of asthma.
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