1. Syntaxin17 Restores Lysosomal Function and Inhibits Pyroptosis Caused by Acinetobacter baumannii.
- Author
-
An Z and Ding W
- Subjects
- Humans, Phosphate-Binding Proteins metabolism, Phosphate-Binding Proteins genetics, Autophagy, Animals, Cathepsin B metabolism, Cathepsin B genetics, Acinetobacter Infections microbiology, Mice, Intracellular Signaling Peptides and Proteins metabolism, Intracellular Signaling Peptides and Proteins genetics, Autophagosomes metabolism, Lysosomal-Associated Membrane Protein 1 metabolism, Gasdermins, Pyroptosis, Lysosomes metabolism, Acinetobacter baumannii metabolism, Acinetobacter baumannii genetics, Interleukin-1beta metabolism, Interleukin-1beta genetics, Qa-SNARE Proteins metabolism, Qa-SNARE Proteins genetics
- 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., (© 2024. The Author(s), under exclusive licence to Microbiological Society of Korea.)
- Published
- 2024
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