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

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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.

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Acknowledgments

We thank Ms. Yoshiko Yamazaki, Michiyo Taguchi, Kumiko Matsuyama for their technical support. This study was partially supported by a Ministry of Education, Science, Sports and Culture Grant-in-Aid for Scientific Research (C), 24591183, 2012.

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Correspondence to Kazuhiro Yatera.

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Akata, K., Yatera, K., Wang, KY. et al. Decreased Bronchial Eosinophilic Inflammation and Mucus Hypersecretion in Asthmatic Mice Lacking All Nitric Oxide Synthase Isoforms. Lung 194, 121–124 (2016). https://doi.org/10.1007/s00408-015-9833-4

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  • DOI: https://doi.org/10.1007/s00408-015-9833-4

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