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万古霉素可阻断巨噬细胞的自噬并诱导白细胞介素-1β释放。

Vancomycin blocks autophagy and induces interleukin-1β release in macrophages.

作者信息

Ha Young Eun, Kong Kyoung-Hye, Cho Mi-Hyang, Kim Dong-Hou, Song Young-Sup, Yoon Seung-Yong

机构信息

Samsung Medical Center, Department of Infectious Diseases, Sungkyunkwan University School of Medicine, Seoul, Korea.

1] Department of Anatomy and Cell Biology, University of Ulsan College of Medicine, Seoul, Korea [2] Cell Dysfunction Research Center (CDRC), Bio-Medical Institute of Technology (BMIT), University of Ulsan College of Medicine, Seoul, Korea.

出版信息

J Antibiot (Tokyo). 2015 Feb;68(2):76-80. doi: 10.1038/ja.2014.112. Epub 2014 Aug 20.

Abstract

Systemic inflammatory response syndrome (SIRS) is a serious condition that can cause organ failure as an exaggerated immunoresponse to the infection or other causes. Recently, autophagy was reported as a key process that regulates inflammatory responses in macrophages. Vancomycin is one of the most commonly prescribed antibiotics for sepsis treatment or following surgery. However, there are no studies on how vancomycin affects autophagy or inflammation. Here, we treated macrophage cell lines with vancomycin and lipopolysaccharides and found that vancomycin blocks autophagy and increases inflammatory responses. This finding suggests that vancomycin should be more cautiously administered in order to prevent unwanted SIRS during sepsis.

摘要

全身炎症反应综合征(SIRS)是一种严重病症,可作为对感染或其他病因的过度免疫反应而导致器官衰竭。最近,自噬被报道为调节巨噬细胞炎症反应的关键过程。万古霉素是脓毒症治疗或术后最常用的抗生素之一。然而,尚无关于万古霉素如何影响自噬或炎症的研究。在此,我们用万古霉素和脂多糖处理巨噬细胞系,发现万古霉素会阻断自噬并增强炎症反应。这一发现表明,为防止脓毒症期间出现不良的全身炎症反应综合征,应更谨慎地使用万古霉素。

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