We found a match
Your institution may have access to this item. Find your institution then sign in to continue.
- Title
Decreased Bronchial Eosinophilic Inflammation and Mucus Hypersecretion in Asthmatic Mice Lacking All Nitric Oxide Synthase Isoforms.
- Authors
Akata, Kentaro; Yatera, Kazuhiro; Wang, Ke-Yong; Naito, Keisuke; Ogoshi, Takaaki; Noguchi, Shingo; Kido, Takashi; Toyohira, Yumiko; Shimokawa, Hiroaki; Yanagihara, Nobuyuki; Tsutsui, Masato; Mukae, Hiroshi
- Abstract
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). Methods: Wild-type and n/i/eNOS mice were sensitized and challenged with ovalbumin. Pathological findings and expressions of interferon (IFN)-γ, interleukin (IL)-4, -5, -10, -13 and chemokines in the lung were evaluated. Results: Decreased 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-γ and IL-10 were similar. Conclusion: Using asthmatic n/i/eNOS mice, NO plays important roles in accelerating bronchial eosinophilic inflammation and mucus hypersecretion in the pathophysiology of asthma.
- Subjects
ASTHMA; AIRWAY (Anatomy); NITRIC-oxide synthases; INTERFERONS; OVALBUMINS; CHEMOKINES; ANIMAL models in research
- Publication
Lung, 2016, Vol 194, Issue 1, p121
- ISSN
0341-2040
- Publication type
Report
- DOI
10.1007/s00408-015-9833-4