2013 Fiscal Year Final Research Report
Mechanisms of mucus overproduction and airway inflammation in asthma
| Project/Area Number |
23790905
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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 | Hamamatsu University School of Medicine |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2013
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| Keywords | 気道炎症 / IL-17C / 気管支喘息 / Toll-like receptor / 粘液過剰産生 / MUC5AC / MUC5B |
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| Research Abstract |
The present study was conducted to elucidate the mechanisms of mucus overproduction and airway inflammation in exacerbation of asthma.
Co-treatment with NF-kappa B activators and STAT6 activators did not show synergistic mucin genes expression in normal human bronchial epithelial (NHBE) cells. We demonstrated that polyI:C, the ligand to Toll-like receptor 3, induced IL-17C expression via TRIF/NF kappa B pathway in NHBE cells. Both IL-17C and polyI:C increased the expression of antimicrobial peptides and proinflammatory cytokines, such as human beta-defensin (hBD) 2, colony-stimulating factor (CSF) 3, and S100A12 in NHBE cells. Knockdown of IL-17 receptor E, the specific receptor for IL-17C, attenuated polyI:C-induced hBD2, CSF3, and S100A12 expression, without any reduction of polyI:C-induced IL-17C expression, which suggest that IL-17C is an essential epithelial cell-derived cytokine that enhances airway inflammation in a unique autocrine/paracrine manner in the airway epithelium.
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