{"title":"Syntaxin17 Restores Lysosomal Function and Inhibits Pyroptosis Caused by Acinetobacter baumannii.","authors":"Zhiyuan An, Wenyi Ding","doi":"10.1007/s12275-024-00109-0","DOIUrl":null,"url":null,"abstract":"<p><p>Acinetobacter baumannii (A. baumannii) causes autophagy flux disorder by degrading STX17, resulting in a serious inflammatory response. It remains unclear whether STX17 can alter the inflammatory response process by controlling autolysosome function. This study aimed to explore the role of STX17 in the regulation of pyroptosis induced by A. baumannii. Our findings indicate that overexpression of STX17 enhances autophagosome degradation, increases LAMP1 expression, reduces Cathepsin B release, and improves lysosomal function. Conversely, knockdown of STX17 suppresses autophagosome degradation, reduces LAMP1 expression, augments Cathepsin B release, and accelerates lysosomal dysfunction. In instances of A. baumannii infection, overexpression of STX17 was found to improve lysosomal function and reduce the expression of mature of GSDMD and IL-1β, along with the release of LDH, thus inhibiting pyroptosis caused by A. baumannii. Conversely, knockdown of STX17 led to increased lysosomal dysfunction and further enhanced the expression of mature of GSDMD and IL-1β, and increased the release of LDH, exacerbating pyroptosis induced by A. baumannii. These findings suggest that STX17 regulates pyroptosis induced by A. baumannii by modulating lysosomal function.</p>","PeriodicalId":16546,"journal":{"name":"Journal of Microbiology","volume":" ","pages":"315-325"},"PeriodicalIF":3.3000,"publicationDate":"2024-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Microbiology","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1007/s12275-024-00109-0","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/3/7 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"MICROBIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Acinetobacter baumannii (A. baumannii) causes autophagy flux disorder by degrading STX17, resulting in a serious inflammatory response. It remains unclear whether STX17 can alter the inflammatory response process by controlling autolysosome function. This study aimed to explore the role of STX17 in the regulation of pyroptosis induced by A. baumannii. Our findings indicate that overexpression of STX17 enhances autophagosome degradation, increases LAMP1 expression, reduces Cathepsin B release, and improves lysosomal function. Conversely, knockdown of STX17 suppresses autophagosome degradation, reduces LAMP1 expression, augments Cathepsin B release, and accelerates lysosomal dysfunction. In instances of A. baumannii infection, overexpression of STX17 was found to improve lysosomal function and reduce the expression of mature of GSDMD and IL-1β, along with the release of LDH, thus inhibiting pyroptosis caused by A. baumannii. Conversely, knockdown of STX17 led to increased lysosomal dysfunction and further enhanced the expression of mature of GSDMD and IL-1β, and increased the release of LDH, exacerbating pyroptosis induced by A. baumannii. These findings suggest that STX17 regulates pyroptosis induced by A. baumannii by modulating lysosomal function.
期刊介绍:
Publishes papers that deal with research on microorganisms, including archaea, bacteria, yeasts, fungi, microalgae, protozoa, and simple eukaryotic microorganisms. Topics considered for publication include Microbial Systematics, Evolutionary Microbiology, Microbial Ecology, Environmental Microbiology, Microbial Genetics, Genomics, Molecular Biology, Microbial Physiology, Biochemistry, Microbial Pathogenesis, Host-Microbe Interaction, Systems Microbiology, Synthetic Microbiology, Bioinformatics and Virology. Manuscripts dealing with simple identification of microorganism(s), cloning of a known gene and its expression in a microbial host, and clinical statistics will not be considered for publication by JM.