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.
Yongchao Guan , Meng Zhang , Yingda Wang , Zhongzhuo Liu , Zelin Zhao , Hong Wang , Dingjie An , Aidong Qian , Yuanhuan Kang , Wuwen Sun , Xiaofeng Shan
J. Microbiol. 2022;60(12):1153-1161. Published online November 10, 2022
Aeromonas veronii is a pathogen which can induce diseases in
humans, animals and aquatic organisms, but its pathogenic
mechanism and virulence factors are still elusive. In this study,
we successfully constructed a mutant strain (ΔascP) by homologous
recombination. The results showed that the deletion
of the ascP gene significantly down-regulated the expression
of associated effector proteins in A. veronii compared
to its wild type. The adhesive and invasive abilities of ΔascP to
EPC cells were 0.82-fold lower in contrast to the wild strain.
The toxicity of ΔascP to cells was decreased by about 2.91-fold
(1 h) and 1.74-fold (2 h). Furthermore, the LD50 of the mutant
strain of crucian carp was reduced by 19.94-fold, and
the virulence was considerably attenuated. In contrast to the
wild strain, the ΔascP content in the liver and spleen was considerably
lower. The titers of serum cytokines (IL-8, TNF-α,
and IL-1β) in crucian carp after the infection of the ΔascP strain
were considerably lower in contrast to the wild strain. Hence,
the ascP gene is essential for the etiopathogenesis of A. veronii
TH0426.
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