The Blockade of IL-17 Attenuates ER Stress in LPS-induced Lung Inflammation

분야: 의약학 > 내과학
저자: ( Yong Chul Lee ) , ( So Ri Kim ) , ( Hee Jung Kim ) , ( Ae Seok Jeong ) , ( Yang Keun Rhee ) , ( Heung Bum Lee ) , ( Seoung Ju Park ) , ( Chi Ryang Chung ) , ( Seung Yong Park ) , ( Dong Im Kim )
발행기관: 대한결핵 및 호흡기학회
간행물정보: 대한결핵및호흡기학회 추계학술발표초록집 2012년, 제114권 209(총1페이지)
파일형식: 0y909925.pdf [무료 PDF 뷰어 다운로드]
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연관 논문

Thematic Poster : TP-31 ; IL-17A Interact with Endoplasmic Reticulum Stress in Bronchial Epithelium of LPS-Induced Acute Lung injury

Thematic Poster : TP-25 ; Inhibition of Interplay between IL-17A and Endoplasmic Reticulum Stress Attenuates LPS-Induced Lung Injury

Free Paper Presentation : F-142 ; Additive Effects of Combined Inhibition of TLR4 and IL-17A on ER stress Liked to Inflammatory Responses in LPS-Induced Acute Lung Injury

Poster Session : PS-1571 ; Pulmonary Infection : IL-17A Interact with Endoplasmic Reticulum Stress in Bronchial Epithelium of LPS-Induced Acute Lung injury

Free Paper Presentation : OS-83 ; Activation of Phosphoinositide 3-Kinase δ Pathway Contributes to Aspergillus Fumigatus-Induced Severe Allergic Asthmatic Inflammation via the Regulation of ER Stress in Mice

영문초록

Pro-inflammatory mediators modulate endoplasmic reticulum (ER) stress, defined as alterations in ER homeostasis under various stress. As a bacterial endotoxin, lipopolysaccharide (LPS) is involved in numerous inflammatory diseases, and IL-17 has been known to be implicated in LPS-induced lung inflammation. However, it is not known exactly how IL-17 interacts with ER stress in LPS-related lung inflammation. In this study, using a murine model of LPS-induced lung inflammation, effects of IL-17 inhibition using anti-IL-17 antibody on LPS-induced lung inflammation were examined, especially in relation to ER stress. Inhibition of IL-17 reduced significantly LPS-induced increases of GRP78 and CHOP protein levels in lung tissues. IL-17 inhibition also lowered LPS-induced increases of unfolded protein response (UPR)-related markers in the lung. Furthermore, increases of airway inflammatory cell infiltrations, vascular leakages, and various pro-inflammatory mediators after LPS treatment were decreased by the neutralization of IL-17. Moreover, administration of 4-phenylbutyrate (PBA), an ER stress inhibitor, attenuated pathologic features as well as increases of various ER stress markers of LPS-induced lung inflammation. And, increases in nuclear translocation of NF-κB p65, expression of Toll-like receptor4 (TLR4), and infiltration of dendritic cells (DCs) into lungs after LPS treatment were reduced after IL-17 blockade. Our results suggest that IL-17 inhibition improves LPS-induced lung inflammation partly through the modulation of ER stress.

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