Abstract：
Aim: Understanding molecular mechanisms of Helicobacter pylori (H. pylori)-induced inflammation is important for developing new therapeutic strategies for gastrointestinal diseases.Materials & methods: We designed an H. pylori-neutrophil infection model and explored the effects of H. pylori infection on neutrophils.Results: H. pylori infected neutrophils showed a low level of apoptosis. H. pylori 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 H. pylori-infected neutrophils.Conclusion: Therefore, H. pylori infection inhibits neutrophils apoptosis and induces IL-1β secretion through autophagy. These findings may be utilized to formulate therapeutic strategies against H. pylori mediated chronic gastritis.
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[Box: see text].
摘要：
目的：了解幽门螺杆菌（H.幽门螺杆菌）诱导的炎症对于开发胃肠道疾病的新治疗策略很重要。材料和方法：我们设计了幽门螺杆菌-中性粒细胞感染模型，并探讨了幽门螺杆菌感染对中性粒细胞的影响。成果：H.pylori沾染的中性粒细胞显示出低水平的凋亡。幽门螺杆菌刺激激活了含NACHT/LRR/PYD结构域的蛋白3（NLRP3）-gasdermin-D（GSDMD）途径，以分泌白介素（IL）-1β。然而,IL-1β的分泌并不完全依赖于GSDMD,由于抑制自噬显著降低了IL-1β的释放，和自噬相关分子在幽门螺杆菌感染的中性粒细胞中显著上调。结论：因此，幽门螺杆菌感染抑制中性粒细胞凋亡并通过自噬诱导IL-1β分泌。这些发现可用于制定针对幽门螺杆菌介导的慢性胃炎的治疗策略。
[方框：见正文]。
[方框：见正文]。
