| Budget Amount *help |
¥2,270,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥270,000)
Fiscal Year 2007: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2006: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Research Abstract |
Since little information is available on eosinophil activation and cytokine response in virus-induced asthma, we attempted to detect respiratory viruses and measure levels of various serum cytokines/chemokines, and eosinophil cationic protein (ECP) in acute as well as stable asthma.
We detected viruses in nasal lavage obtained from patients with acute asthma using antigen detection kits or PCR followed by direct DNA sequencing analysis. We also measured peripheral eosinophil counts, concentrations of serum ECP, and 17 types of cytokines/chemokines (IL-1J3, 2, 4, 5, 6, 7, 8, 10, 12, 13, 17, IFN-γ, TNF-α, GM-CSF, G-CSF, MCP-1, and MIP-1β) using a multiplex beads-based assay (Bio-Rad) in 38 patients with acute asthma and in 51 patients with stable asthma who were not taking systemic corticosteroids. We also investigated the high expression gene in human stimulated eosinophils from patients with asthma using a gene microarray analysis (Affymetrix).
Of the 157 acute asthma, rhinovirus was det
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ected in 46; RS virus, in 43; enterovirus, in 18; other viruses, in 18; and no viruses, in 32. The concentrations of ECP, IL-5, 6, 8, and IL-10, but not eosinophil counts, were significantly elevated in acute asthma as compared with those in stable asthma. These results were more similar to those observed in rhinovirus-induced asthma and RS virus-induced asthma than to those of stable asthma. Only the IL-5 level was significantly elevated in the rhinovirus group than in the RS virus. Finally, we found that several genes including caspase 4, serine/threonine kinase 17b, chemokine (C-C motif)ligand 5, chemokine (C-C motif) receptor 1 upregulated in human stimulated eosinophils obtained by asthmatic patients.
The major causes of respiratory virus-induced childhood asthma were rhinovirus and RS virus.
Virus-induced asthma, particularly those induced by rhinoviruses, might enhance eosinophil activation.
Furthermore, these genes might be a therapeutic target for eosinophilic inflammation in asthma. Less
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