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2 "Cathepsin B"
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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
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AbstractAbstract
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.
Weigela florida inhibits the expression of inflammatory mediators induced by Pseudomonas aeruginosa and Staphylococcus aureus infection
Hyo Bin Kim , Soomin Cho , Yeji Lee , Weihui Wu , Un-Hwan Ha
J. Microbiol. 2022;60(6):649-656.   Published online April 30, 2022
DOI: https://doi.org/10.1007/s12275-022-1638-6
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AbstractAbstract
Inflammatory responses involve the action of inflammatory mediators that are necessary for the clearance of invading bacterial pathogens. However, excessive production of inflammatory mediators can damage tissues, thereby impairing bacterial clearance. Here, we examined the effects of Weigela florida on the expression of inflammatory cytokines induced by Pseudomonas aeruginosa or Staphylococcus aureus infection in macrophages. The results showed that pre-treatment with W. florida markedly downregulated the bacterial infectionmediated expression of cytokines. Additionally, post-treatment also triggered anti-inflammatory effects in cells infected with S. aureus to a greater extent than in those infected with P. aeruginosa. Bacterial infection activated inflammation-associated AKT (Thr308 and Ser473)/NF-κB and MAPK (p38, JNK, and ERK) signaling pathways, whereas W. florida treatment typically inhibited the phosphorylation of AKT/NF‐κB and p38/JNK, supporting the anti‐inflammatory effects of W. florida. The present results suggest that W. florida decreases the infection-mediated expression of inflammatory mediators by inhibiting the AKT/NF-κB and MAPK signaling pathways, implying that it may have potential use as an inhibitory agent of excessive inflammatory responses.

Citations

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