IL-17 Regulates ER Stress in Neutrophilic Bronchial Asthma
분야
의약학 > 내과학
저자
( Jae Seok Jeong ) , ( Yong Chul Lee ) , ( So Ri Kim ) , ( Hee Jung Kim ) , ( Yang Keun Rhee ) , ( Heung Bum Lee ) , ( Seoung Ju Park ) , ( Chi Ryang Chung ) , ( Seung Yong Park ) , ( Dong Im Kim ) , ( Kyung Sun Lee )
발행기관
대한결핵 및 호흡기학회
간행물정보
대한결핵및호흡기학회 추계학술발표초록집 2012년, 제114권 189(총1페이지)
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    영문초록
    IL-17 has been increasingly known to be implicated in the pathogenesis of asthma as a pro-inflammatory regulator by inducing the expression of various inflammatory mediators. Recent studies have demonstrated that excess of endoplasmic reticulum (ER) stress interferes with protein synthesis and secretion, induces reactive oxygen species generation, increases inflammation via NF-kB activation, and mediates apoptotic cell death through the expression of CHOP, thereby being involved in various disorders. In addition, while various inflammatory stimuli can induce the excess of ER stress, there is little information dealing with the relationship between IL-17 and ER stress in airway inflammatory disorders. In this study, we have evaluated the interaction between IL-17 and ER stress using a murine model of asthma. The OVALPS-OVA mice showed that the expression of ER stress markers and the protein levels of unfolded-protein response (UPR)-related marker in lung tissues were significantly increased after OVA challenge. Our results also showed that IL-17 neutralizing antibody significantly reduced the increases in ER stress, inflammatory cytokines, airway inflammation, and bronchial hyperresponsiveness. Moreover, our data showed that 4-phenylbutyric acid (4-PBA), a chemical chaperone significantly reduced the increases in ER stress, inflammatory cytokines, airway inflammation, and bronchial hyperresponsiveness. These findings suggest that IL-17 plays an important role in the pathogenesis of bronchial asthma, at least in part, through the modulation of ER stress.
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