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dc.contributor.authorLee, Yi-Chenen_US
dc.contributor.authorLin, Chun-Yuen_US
dc.contributor.authorChen, Yen-Hsuen_US
dc.contributor.authorChiu, Wen-Chinen_US
dc.contributor.authorWang, Yen-Yunen_US
dc.contributor.authorHsu, Chinen_US
dc.contributor.authorHu, Stephen Chu-Sungen_US
dc.contributor.authorSu, Yu-Hanen_US
dc.contributor.authorYuan, Shyng-Shiou F.en_US
dc.date.accessioned2019-06-03T01:08:36Z-
dc.date.available2019-06-03T01:08:36Z-
dc.date.issued2019-04-04en_US
dc.identifier.issn1422-0067en_US
dc.identifier.urihttp://dx.doi.org/10.3390/ijms20071678en_US
dc.identifier.urihttp://hdl.handle.net/11536/151968-
dc.description.abstractAcute lung injury (ALI) is a life-threatening syndrome characterized by acute and severe hypoxemic respiratory failure. Visfatin, which is known as an obesity-related cytokine with pro-inflammatory activities, plays a role in regulation of inflammatory cytokines. The mechanisms of ALI remain unclear in critically ill patients. Survival in ALI patients appear to be influenced by the stress generated by mechanical ventilation and by ALI-associated factors that initiate the inflammatory response. The objective for this study was to understand the mechanisms of how visfatin regulates inflammatory cytokines and promotes ALI. The expression of visfatin was evaluated in ALI patients and mouse sepsis models. Moreover, the underlying mechanisms were investigated using human bronchial epithelial cell lines, BEAS-2B and NL-20. An increase of serum visfatin was discovered in ALI patients compared to normal controls. Results from hematoxylin and eosin (H&E) and immunohistochemistry staining also showed that visfatin protein was upregulated in mouse sepsis models. Moreover, lipopolysaccharide (LPS) induced visfatin expression, activated the STAT3/NF kappa B pathway, and increased the expression of pro-inflammatory cytokines, including IL1-beta, IL-6, and TNF-alpha in human bronchial epithelial cell lines NL-20 and BEAS-2B. Co-treatment of visfatin inhibitor FK866 reversed the activation of the STAT3/NF kappa B pathway and the increase of pro-inflammatory cytokines induced by LPS. Our study provides new evidence for the involvement of visfatin and down-stream events in acute lung injury. Further studies are required to confirm whether the anti-visfatin approaches can improve ALI patient survival by alleviating the pro-inflammatory process.en_US
dc.language.isoen_USen_US
dc.subjectacute lung injuryen_US
dc.subjectvisfatinen_US
dc.subjectFK866en_US
dc.titleEssential Role of Visfatin in Lipopolysaccharide and Colon Ascendens Stent Peritonitis-Induced Acute Lung Injuryen_US
dc.typeArticleen_US
dc.identifier.doi10.3390/ijms20071678en_US
dc.identifier.journalINTERNATIONAL JOURNAL OF MOLECULAR SCIENCESen_US
dc.citation.volume20en_US
dc.citation.issue7en_US
dc.citation.spage0en_US
dc.citation.epage0en_US
dc.contributor.department交大名義發表zh_TW
dc.contributor.department生醫工程研究所zh_TW
dc.contributor.departmentNational Chiao Tung Universityen_US
dc.contributor.departmentInstitute of Biomedical Engineeringen_US
dc.identifier.wosnumberWOS:000464977600017en_US
dc.citation.woscount0en_US
Appears in Collections:Articles