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.

Anti-tumor Activity of the Fruitbody Extract of Basidiomycete, Phellinus linteus: Jong-Soon Lim , Seung-Hyung Kim , Jin-Seo Park , Jeong-Youl Choi , Seong Joo Park , Kwang-Soo Shin; J. Microbiol. 2001;39(2):121-125.

Abstract: Methanol extract prepared from the fruitbody of Phellinus linteus (EPL) showed anti-tumor and immuno-stimulating activities. The invasion activity of B16-F10 melanoma cells through a reconstituted basement membrane to the collagen-coated lower surface of the filters was inhibited about 67% by EPL (100 ug/ml). Also, EPL inhibited the expression of the mRNA for MMP-2 and MMP-9. In vivo treatment of C57BL/6 mice (150 mg/kg) with EPL for 14 days, the pulmonary colonization was found to be inhibited about 75%. Using reverse transcriptionpolymerase chain reaction (RT-PCR) analysis, we found that cytokine IL-12 and INF-[gamma] genes were induced by EPL. Furthermore, EPL stimulated the proliferation of CD4^+ (33.5%) and CD8^+ (17.7%) in mouse splenocytes.

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