{Reference Type}: Journal Article
{Title}: Helicobacter pylori infection delays neutrophil apoptosis and exacerbates inflammatory response.
{Author}: Song Y;Liu P;Qi X;Shi XL;Wang YS;Guo D;Luo H;Du ZJ;Wang MY;
{Journal}: Future Microbiol
{Volume}: 19
{Issue}: 13
{Year}: 2024 Sep 26
{Factor}: 3.553
{DOI}: 10.1080/17460913.2024.2360798
{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.<BR>[Box: see text].