2009 Fiscal Year Final Research Report
The disruption mechanism of innate immune system in RSV infected epithelial cells and search of its restoration compound.
| Project/Area Number |
20790356
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Virology
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
OKABAYASHI Tamaki Sapporo Medical University, 医学部, 講師 (10359995)
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| Project Period (FY) |
2008 – 2009
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| Keywords | 病原性 |
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| Research Abstract |
Respiratory syncytial virus (RSV) is one of the most common causes of respiratory diseases in children. Nasal epithelial cell (NEC) is the first site exposure to RSV. NEC induced type-III IFN by RSV infection, but not merely type-I IFN. Our results showed that RIG-I, one of the virus sensors, contributed to this type-III IFN production. Fosfomycin, anti-bacterial agent, suppressed the RSV-induced a proinflammatory chemokine, RANTES production, and a receptor for Streptococcus pneumoniae, platelet-activating factor receptor expression, by inhibition of transcription factor NF-κB activity.
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