Yu Song, Peng Liu, Xi Qi, Xiao-Lin Shi, Yu-Shan Wang, Dong Guo, Hong Luo, Zong-Jun Du, Ming-Yi Wang
{"title":"<i>Helicobacter pylori</i> infection delays neutrophil apoptosis and exacerbates inflammatory response.","authors":"Yu Song, Peng Liu, Xi Qi, Xiao-Lin Shi, Yu-Shan Wang, Dong Guo, Hong Luo, Zong-Jun Du, Ming-Yi Wang","doi":"10.1080/17460913.2024.2360798","DOIUrl":null,"url":null,"abstract":"<p><p><b>Aim:</b> Understanding molecular mechanisms of <i>Helicobacter pylori</i> (<i>H. pylori</i>)-induced inflammation is important for developing new therapeutic strategies for gastrointestinal diseases.<b>Materials & methods:</b> We designed an <i>H. pylori</i>-neutrophil infection model and explored the effects of <i>H. pylori</i> infection on neutrophils.<b>Results:</b> <i>H. pylori</i> infected neutrophils showed a low level of apoptosis. <i>H. pylori</i> 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 <i>H. pylori</i>-infected neutrophils.<b>Conclusion:</b> Therefore, <i>H. pylori</i> infection inhibits neutrophils apoptosis and induces IL-1β secretion through autophagy. These findings may be utilized to formulate therapeutic strategies against <i>H. pylori</i> mediated chronic gastritis.</p>","PeriodicalId":2,"journal":{"name":"ACS Applied Bio Materials","volume":null,"pages":null},"PeriodicalIF":4.6000,"publicationDate":"2024-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11529197/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"ACS Applied Bio Materials","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1080/17460913.2024.2360798","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/7/26 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"MATERIALS SCIENCE, BIOMATERIALS","Score":null,"Total":0}
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.