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Free Paper Presentation : OS-118 ; Cigarette Smoke Extract Enhances IL-17A-Induced IL-8 Production in Normal Human Bronchial Epithelial Cells, Which Is Mediated in Part by Up-Regulation of IL-17RA and IL-17RC
( Eun Sun Kim ) , ( Kyoung Hee Lee ) , ( Ji Yeong Jeong ) , ( Chang Hoon Lee ) , ( Chul Gyu Yoo )
UCI I410-ECN-0102-2015-500-002124365
This article is 4 pages or less.
* This article is free of use.

Background: Cigarette smoke and interleukin-17A (IL-17A) are involved in inflammatory airway diseases, and the mechanisms behind these processes are still poorly understood. We investigated if recombinant human IL-17A in combination with cigarette smoke extract (CSE) increases the level of inflammatory cytokine and if CSE has effect on the expression of IL-17A receptor in normal human bronchial epithelial cells. Methods: BEAS-2B cells were used. IL-8 mRNA expression was determined by real-time PCR and released IL-8 in culture supernatant was measured by ELISA. IL-17 receptor A (IL-17RA) and IL-17RC expressions were evaluated by real-time PCR, Western blot analysis, or FACS. Results: IL-17A increased IL-8 transcripts and the release of IL-8 in a dose-dependent manner. CSE treatment significantly enhanced IL-17A-mediated IL-8 production. CSE induced both IL-17RA and IL-17RC mRNA expression and increased protein expression of both receptors in total cellular lysates. CSE up-regulated the expression of surface membrane IL-17RA. Conclusions: CSE enhances IL-17A-induced IL-8 production. Increased IL-17RA and IL-17RC by CSE might contribute to this enhanced inflammatory response.

[자료제공 : 네이버학술정보]
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