Helicobacter pylori infection delays neutrophil apoptosis and exacerbates inflammatory response.

IF 2.5 4区 生物学 Q3 MICROBIOLOGY
Future microbiology Pub Date : 2024-09-01 Epub Date: 2024-07-26 DOI:10.1080/17460913.2024.2360798
Yu Song, Peng Liu, Xi Qi, Xiao-Lin Shi, Yu-Shan Wang, Dong Guo, Hong Luo, Zong-Jun Du, Ming-Yi Wang
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引用次数: 0

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.

幽门螺杆菌感染会延缓中性粒细胞凋亡并加剧炎症反应。
目的:了解幽门螺杆菌(H. pylori)诱导炎症的分子机制对于开发新的胃肠道疾病治疗策略非常重要。材料与方法: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。结果幽门螺杆菌感染的中性粒细胞凋亡水平较低。幽门螺杆菌刺激激活了 NACHT/LRR/PYD domain-containing protein 3 (NLRP3)-gasdermin-D (GSDMD) 通路,导致白细胞介素(IL)-1β分泌。然而,IL-1β的分泌并不完全依赖于GSDMD,因为抑制自噬可显著减少IL-1β的释放,而且幽门螺杆菌感染的中性粒细胞中自噬相关分子显著上调。结论因此,幽门螺杆菌感染可抑制中性粒细胞凋亡,并通过自噬诱导 IL-1β 的分泌。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。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Future microbiology
Future microbiology 生物-微生物学
CiteScore
4.90
自引率
3.20%
发文量
134
审稿时长
6-12 weeks
期刊介绍: Future Microbiology delivers essential information in concise, at-a-glance article formats. Key advances in the field are reported and analyzed by international experts, providing an authoritative but accessible forum for this increasingly important and vast area of research.
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