TY - JOUR
T1 - Decreased Bronchial Eosinophilic Inflammation and Mucus Hypersecretion in Asthmatic Mice Lacking All Nitric Oxide Synthase Isoforms
AU - Akata, Kentaro
AU - Yatera, Kazuhiro
AU - Wang, Ke Yong
AU - Naito, Keisuke
AU - Ogoshi, Takaaki
AU - Noguchi, Shingo
AU - Kido, Takashi
AU - Toyohira, Yumiko
AU - Shimokawa, Hiroaki
AU - Yanagihara, Nobuyuki
AU - Tsutsui, Masato
AU - Mukae, Hiroshi
N1 - Funding Information:
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.
Publisher Copyright:
© 2015, Springer Science+Business Media New York.
PY - 2016/2/1
Y1 - 2016/2/1
N2 - 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.
AB - 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.
KW - Bronchial asthma
KW - Eosinophilic inflammation
KW - Nitric oxide
KW - Nitric oxide synthase
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U2 - 10.1007/s00408-015-9833-4
DO - 10.1007/s00408-015-9833-4
M3 - Article
C2 - 26685897
AN - SCOPUS:84957850493
VL - 194
SP - 121
EP - 124
JO - Pneumonologie. Pneumonology
JF - Pneumonologie. Pneumonology
SN - 0341-2040
IS - 1
ER -