2007 Fiscal Year Final Research Report Summary
Respiratory Syncytial Virus (RSV) infection inhibits lung eosinophilia, but induces profound eosinophil degranulation in allergic mice
| Project/Area Number |
17591805
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Nippon Medical School |
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Principal Investigator |
TAKIZAWA Ryuta Nippon Medical School, Dept. of Otolaryngology, Assistant professor (10271347)
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| Co-Investigator(Kenkyū-buntansha) |
RUBY Pawankar Nippon Medical School, Dept. of Otolaryngology, Associate professor (00287674)
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| Project Period (FY) |
2005 – 2007
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| Keywords | Allergy / RSV / Cytokine / Chemokine / Mouse |
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| Research Abstract |
RSV-induced bronchiolitis in infants is characterized by high concentrations of eosinophil-derived proteins, including ECP, MBP, and EDN, in nasal and tracheal aspirates. However, attempts to demonstrate the presence of eosinophils in airway mucosa or secretions of infants with RSV infections have been unsuccessful.
A BALB/c mouse model of lung eosinophilia (OVA-induced) was used. OVA-sensitized, challenged (by repeated OVA nebulization) mice were infected with RSV or sham-inoculated and differential cell counts were performed in cells recovered by bronchoalveolar lavage (BAL) at day 1 after RSV or sham inoculation. Eosinophil peroxidase (EPO) activity in the BAL fluid was measured by a specific colorimetric assay.
A significant reduction in the number of BAL eosinophils was observed in RSV-infected OVA-challenged mice (1.3×10^5/ml) compared with sham-infected, OVA-challenged mice (4.0×10^5/m1) (p<0.001). OVA-challenged, sham infected mice had no evidence of eosinophil degranulation, as no detectable EPO activity was present in the BAL fluid. On the other hand, OVA-challenged, RSV-infected mice had high levels of EPO activity in BAL fluid (p<0.01).
These findings suggest the existence of a complex interplay between RSV infection and the migratory and activation pathways of eosinophils that may affect the response of atopic as well as non-atopic individuals to respiratory viral infections.
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