title: Vancomycin blocks autophagy and induces interleukin-1β release in macrophages.
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.
authors.affiliation: Samsung Medical Center, Department of Infectious Diseases, Sungkyunkwan University School of Medicine, Seoul, Korea.
authors.forename: Young Eun
authors.initials: YE
authors.lastname: Ha
authors.affiliation: 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.
authors.forename: Kyoung-Hye
authors.initials: KH
authors.lastname: Kong
authors.affiliation: 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.
authors.forename: Mi-Hyang
authors.initials: MH
authors.lastname: Cho
authors.affiliation: 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.
authors.forename: Dong-Hou
authors.initials: DH
authors.lastname: Kim
authors.affiliation: 1] Cell Dysfunction Research Center (CDRC), Bio-Medical Institute of Technology (BMIT), University of Ulsan College of Medicine, Seoul, Korea [2] Department of Biomedical Sciences, University of Ulsan College of Medicine, Seoul, Korea.
authors.forename: Young-Sup
authors.initials: YS
authors.lastname: Song
authors.affiliation: 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.
authors.forename: Seung-Yong
authors.initials: SY
authors.lastname: Yoon
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D001343:Autophagy / Q000187:drug effects*; D002460:Cell Line; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000276:immunology; D053583:Interleukin-1beta / Q000187:drug effects* / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D008264:Macrophages / Q000187:drug effects* / Q000276:immunology; D051379:Mice; D018805:Sepsis / Q000188:drug therapy / Q000276:immunology; D018746:Systemic Inflammatory Response Syndrome / Q000276:immunology / Q000517:prevention & control; D014640:Vancomycin / Q000494:pharmacology*
chemical_list: D000900:Anti-Bacterial Agents; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D014640:Vancomycin