鲍曼不动杆菌(A.鲍曼不动杆菌)通过降解STX17引起自噬通量紊乱,导致严重的炎症反应。尚不清楚STX17是否可以通过控制自身溶酶体功能来改变炎症反应过程。本研究旨在探讨STX17在鲍曼不动杆菌诱导的焦亡中的作用。我们的发现表明STX17的过表达增强了自噬小体的降解,增加LAMP1表达,减少组织蛋白酶B的释放,并改善溶酶体功能。相反,STX17的敲低抑制自噬体降解,减少LAMP1表达,增加组织蛋白酶B的释放,加速溶酶体功能障碍.在鲍曼不动杆菌感染的情况下,发现STX17的过表达可以改善溶酶体功能并降低GSDMD和IL-1β的成熟表达,随着LDH的释放,从而抑制鲍曼不动杆菌引起的焦亡。相反,STX17基因敲除导致溶酶体功能异常增加,并进一步增强成熟GSDMD和IL-1β的表达,并增加了LDH的释放,加重鲍曼不动杆菌诱导的焦亡。这些发现表明STX17通过调节溶酶体功能来调节鲍曼不动杆菌诱导的焦亡。
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.