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.
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.
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