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The interleukin8 and NF(nuclear factor)-kB in rhinovirus-induced airway inflammation
| DC Field | Value | Language |
|---|---|---|
| dc.contributor.author | 김태형 | - |
| dc.date.accessioned | 2021-08-04T06:03:11Z | - |
| dc.date.available | 2021-08-04T06:03:11Z | - |
| dc.date.issued | 2004-03-31 | - |
| dc.identifier.uri | https://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/74675 | - |
| dc.description.abstract | Background: Since the rhinovirus(RV) does not directly destroy the airway epithelium, it is presumed that the immune response to the RV contributes to the pathogenesis of the respiratory symptoms. In order to test this hypothesis, we characterized time-sequenced alterations in interleukin(IL)-8 elaboration fromthe human epithelial cells and evaluated the role of NF(nuclear factor)-kB in the RV-induced IL-8 production by pretreating the inhibitors of NF-kB activation.Methods: This study nifected BEAS-2B cells with the RV14. The supernatants were harvested from the RV infected BEAS-2B cells and the controls at 2hr, 4hr, 6hr, 12hr, 24hr, 48hr from the inoculation time. Also, the effect fo NF-kB inhibitors was evaluated on RV-induced IL-8 productions. Results: The BEAS-2B cells produced small amounts of IL-8 that accumulated slowly with time in the culture. The RV was a potent stimulator of the IL-8 proteins production by BEAS-2B cells. Antioxidants, N-acetyl-L-cysteine(NAC) and pyrrolidine dithiocarbamate(PDTC), blocked the IL-8 elaboration by the RV-infected BEAS-2B cells, which was dose-dependent, but N-Tosyl-L-phenylalanine chloromethyl ketone(TPCK) did not. Conclusion: Some antioxidants inhibit the RV-induced IL-8 production by blocking NF-kB, which may have a therapeutic potential in asthma. | - |
| dc.title | The interleukin8 and NF(nuclear factor)-kB in rhinovirus-induced airway inflammation | - |
| dc.type | Conference | - |
| dc.citation.conferenceName | 제 44회 일본호흡기학회학술강연회 | - |
| dc.citation.conferencePlace | 일본 | - |
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