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


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2015-12-19

AUTHORS

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

ABSTRACT

BackgroundAsthma 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)-γ, 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-γ 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. More... »

PAGES

121-124

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00408-015-9833-4

DOI

http://dx.doi.org/10.1007/s00408-015-9833-4

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1046238522

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/26685897


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30 schema:description BackgroundAsthma 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)-γ, 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-γ 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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36 schema:keywords BackgroundAsthma
37 ConclusionUsing
38 IFN
39 IL-10
40 IL-4
41 MethodsWild-type
42 NO
43 NO/NOS
44 NOS
45 NOS inhibitor
46 NOS knockout mice
47 activation-regulated chemokine expression
48 airflow limitation
49 airway inflammation
50 asthma
51 asthmatic mice
52 authentic role
53 bronchial eosinophilic inflammation
54 bronchial thickening
55 chemoattractant protein-1
56 chemokine expression
57 chemokines
58 chronic airway inflammation
59 eosinophilic inflammation
60 eotaxin-1
61 expression
62 expression of IFN
63 expression of interferon
64 findings
65 hyperresponsiveness
66 hypersecretion
67 important role
68 inflammation
69 inhibitors
70 interferon
71 interleukin
72 isoforms
73 limitations
74 lung
75 mice
76 mucus hypersecretion
77 mucus secretion
78 nitric oxide synthase isoforms
79 ovalbumin
80 pathological findings
81 pathophysiology
82 pathophysiology of asthma
83 protein 1
84 results
85 role
86 secretion
87 synthase isoforms
88 thickening
89 thymus
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