Journal of Microbiology

Journal Article

Syntaxin17 Restores Lysosomal Function and Inhibits Pyroptosis Caused by Acinetobacter baumannii.: Zhiyuan An, Wenyi Ding; J. Microbiol. 2024;62(4):315-325. Published online March 7, 2024; DOI: https://doi.org/10.1007/s12275-024-00109-0

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.

Research Support, Non-U.S. Gov't

Lactobacillus delbrueckii ssp. lactis R4 Prevents Salmonella typhimurium SL1344-Induced Damage to Tight Junctions and Adherens Junctions: Qinghua Yu , Liqi Zhu , Zhisheng Wang , Pengcheng Li , Qian Yang; J. Microbiol. 2012;50(4):613-617. Published online August 25, 2012; DOI: https://doi.org/10.1007/s12275-012-1596-5

Abstract: Cell junctions are the gatekeepers of the paracellular route and defend the mucosal barrier. Several enteropathogenic bacteria can invade intestinal epithelial cells by targeting and damaging cell junctions. It is not well understood how Salmonella typhimurium is able to overcome the intestinal barrier and gain access to the circulation, nor is it understood how Lactobacillus prevents the invasion of S. typhimurium. Therefore, we sought to determine whether infection with S. typhimurium SL1344 could regulate the molecular composition of cell junctions and whether Lactobacillus delbrueckii ssp. lactis R4 could affect this modification. Our data demonstrated that infection of Caco-2 cells with S. typhimurium over 2 h resulted in a redistribution of claudin-1, ZO-1, occluding, and E-cadherin. Western blot analysis of epithelial cell lysates demonstrated that S. typhimurium could decrease the expression of cell junction proteins. However, L. delbrueckii ssp. lactis R4 ameliorated this destruction and induced increased expression of ZO-1, occludin, and E-cadherin relative to the levels in the control group. The results of these experiments implied that S. typhimurium may facilitate its uptake and distribution within the host by regulating the molecular composition of cell junctions. Furthermore, Lactobacillus may prevent the adhesion and invasion of pathogenic bacteria by maintaining cell junctions and the mucosal barrier.

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