2016 Fiscal Year Final Research Report
Dysfunction of Siglec regulated eosinophilic airway inflammation induce airway remodeling.
| Project/Area Number |
26860596
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | University of Tsukuba |
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Principal Investigator |
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Keywords | Siglec-F / 気道リモデリング / HAS2 / Siglec / Muc5b / Muc4 |
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| Outline of Final Research Achievements |
We studied the influence of Siglec pathway on airway remodeling, which is a refractory factor of bronchial asthma. Siglec is a sugar chain-binding protein mainly expressed in inflammatory cells, mouse Siglec-F is mainly expressed on eosinophils. Muc 5b and Muc 4 were identified as ligands for Siglec-F. In addition, the expression level of Siglec-F ligand was increased when airway remodeling was progressed. Hyaluronan synthase HAS2 dysfunction seemed to inhibit the Siglec pathway and may induce refractory asthma.
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| Free Research Field |
呼吸器内科学
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