Marine College, Shandong University, Weihai, Shandong, 264209, PR China.
Department of Central Lab, Weihai Municipal Hospital, Shandong University, Weihai, Shandong, 264200, PR China.
Future Microbiol. 2024 Sep;19(13):1145-1156. doi: 10.1080/17460913.2024.2360798. Epub 2024 Jul 26.
Understanding molecular mechanisms of ()-induced inflammation is important for developing new therapeutic strategies for gastrointestinal diseases. We designed an -neutrophil infection model and explored the effects of infection on neutrophils. infected neutrophils showed a low level of apoptosis. stimulation activated the NACHT/LRR/PYD domain-containing protein 3 (NLRP3)-gasdermin-D (GSDMD) pathway for interleukin (IL)-1β secretion. However, IL-1β secretion was not completely dependent on GSDMD, as inhibition of autophagy significantly reduced IL-1β release, and autophagy-related molecules were significantly upregulated in -infected neutrophils. Therefore, infection inhibits neutrophils apoptosis and induces IL-1β secretion through autophagy. These findings may be utilized to formulate therapeutic strategies against mediated chronic gastritis.
了解 () 诱导炎症的分子机制对于开发胃肠道疾病的新治疗策略非常重要。我们设计了一种 - 中性粒细胞感染模型，探讨了 感染对中性粒细胞的影响。 感染的中性粒细胞表现出低水平的细胞凋亡。 刺激激活 NACHT/LRR/PYD 结构域包含蛋白 3 (NLRP3)-gasdermin-D (GSDMD) 通路，导致白细胞介素 (IL)-1β 分泌。然而，IL-1β 分泌并不完全依赖于 GSDMD，因为自噬的抑制显著降低了 IL-1β 的释放，并且自噬相关分子在 感染的中性粒细胞中显著上调。因此， 感染通过自噬抑制中性粒细胞凋亡并诱导 IL-1β 分泌。这些发现可能被用于制定针对 介导的慢性胃炎的治疗策略。
