Decreased Bronchial Eosinophilic Inflammation and Mucus Hypersecretion in Asthmatic Mice Lacking All Nitric Oxide Synthase Isoforms

Kentaro Akata, Kazuhiro Yatera, Ke Yong Wang, Keisuke Naito, Takaaki Ogoshi, Shingo Noguchi, Takashi Kido, Yumiko Toyohira, Hiroaki Shimokawa, Nobuyuki Yanagihara, Masato Tsutsui, Hiroshi Mukae

Research output: Contribution to journalArticlepeer-review

6 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)121-124
Number of pages4
JournalLung
Volume194
Issue number1
DOIs
Publication statusPublished - 2016 Feb 1

Keywords

  • Bronchial asthma
  • Eosinophilic inflammation
  • Nitric oxide
  • Nitric oxide synthase

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine

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