Helicobacter pylori infection delays neutrophil apoptosis and exacerbates inflammatory response.
Future Microbiol
; : 1-12, 2024 Jul 26.
Article
de En
| MEDLINE
| ID: mdl-39056165
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)-1ß secretion. However, IL-1ß secretion was not completely dependent on GSDMD, as inhibition of autophagy significantly reduced IL-1ß release, and autophagy-related molecules were significantly upregulated in H. pylori-infected neutrophils.Conclusion:
Therefore, H. pylori infection inhibits neutrophils apoptosis and induces IL-1ß secretion through autophagy. These findings may be utilized to formulate therapeutic strategies against H. pylori mediated chronic gastritis.
[Box see text].
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Langue:
En
Journal:
Future Microbiol
Sujet du journal:
MICROBIOLOGIA
Année:
2024
Type de document:
Article