| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1996: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1995: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Research Abstract |
Exacerbations of bronchial asthma are often associated with respiratory infection caused by rhinovirus infection. To examine the rhinovirus infection on respiratory epithelium, a primary target for respiratory viruses, human rhinovirus 14 (HRV-14) was infected to cultures from the human tracheal epithelium. Viral infection was confirmed by showing that viral titers of supernatants infcreased with time. HRV-14 infection up-regulated the intercellular adhesion molecule-1 (ICAM-1) mRNA,the receptor for the virus, on epithelial cells and it increased the production of IL-1beta, IL-6, IL-8 and TNF-alpha in supernatants. Hemin up-regulated the heme oxygenase 1 (HO-1) mRNA expression on epithelial cells and reduced the viral titers of supernatants. The decreased viral titers of supernatants were then increased by Sn protoporphyrin IX (SnPP9), a specific inhibitor for HO-1. Furthermore, HRV-14 was infected to cultures of human tracheal submucosal glands and HRV-14 titers of supernatants increased with time. HRV-14 up-regulated production of ICAM-1 and IL-1beta, IL-6, IL-8, TNF-alpha and GM-CSF by the cultured human tracheal submucosal glands. These results suggest that up-regulation of cytokines and ICAM-1 production by the cells of airway epithelium and submucosal glands may relate to airway inflammation after rhinovirus infection, and that HO-1 may have a protective effect against rhinovirus infection.
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