Human bronchial epithelial cells produce Semaphorin 3A; possible involvement of Semaphorin 3A in neutrophilic airway inflammation
| Project/Area Number |
24591554
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Saga University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
谷口 一登 佐賀大学, 医学部, 助教 (20625347)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 気道上皮細胞 / ウイルス気道感染 / 気道炎症 / 神経原性炎症 / Semaphorin |
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| Outline of Final Research Achievements |
Semaphorin 3A (Sema3A) has been originally known as the axonal guidance cue in the nerve system. However, the expression of Sema3A in the airway is unknown. This study investigated the expression and the role of Sema3A in the airway.
A human bronchial epithelial cells, BEAS-2B and NHBE, showed constitutive mRNA expression and protein production of Sema3A. Poly inocinic-citydiric acid (poly(IC)), enhanced both mRNA expression and protein production of Sema3A in a dose dependent manner. As neutrophils express Sema3A receptors, we postulated that Sema3A produced from bronchial epithelial cells might modulate functions of neutrophils. Although Sema3A showed no effects on apoptosis and migration of neutrophils, Sema3A enhanced phagocytosis of neutrophils. These findings demonstrate that airway epithelial cells produce Sema3A, and suggest a possibility that Sema3A might modulate a pathogenesis of viral airway infections through up-regulation of phagocytosis of neutrophils.
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Report
(4 results)
Research Products
(2 results)
