Anti-inflammatory effects of extracellular vesicles and cell-free supernatant derived from Lactobacillus crispatus strain RIGLD-1 on Helicobacter pylori-induced inflammatory response in gastric epithelial cells in vitro
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View abstract on PubMed
Summary
This summary is machine-generated.Lactobacillus crispatus extracellular vesicles (EVs) and cell-free supernatant (CFS) can reduce inflammation caused by Helicobacter pylori infection. These compounds show potential as novel therapeutic agents for managing H. pylori-triggered inflammatory responses.
Area Of Science
- Microbiology
- Immunology
- Gastroenterology
Background
- Helicobacter pylori infection is a primary cause of gastric cancer.
- Managing H. pylori infection often involves antibiotics, probiotics, and postbiotics.
Purpose Of The Study
- To investigate the immunomodulatory effects of Lactobacillus crispatus-derived extracellular vesicles (EVs) and cell-free supernatant (CFS) on H. pylori-induced inflammation in gastric cells.
Main Methods
- Isolation and characterization of L. crispatus EVs (ultracentrifugation, DLS, TEM, SEM, SDS-PAGE).
- Assessment of cell viability (MTT assay).
- Quantification of inflammatory gene mRNA expression (RT-qPCR) and IL-8 protein production (ELISA) in AGS cells.
Main Results
- L. crispatus EVs and CFS modulated H. pylori-induced inflammation by downregulating pro-inflammatory cytokines (IL-1β, IL-6, IL-8, TNF-α) and upregulating anti-inflammatory cytokines (IL-10, TGF-β).
- H. pylori-induced IL-8 production was significantly reduced by L. crispatus EVs and CFS treatment.
Conclusions
- L. crispatus strain RIGLD-1 derived EVs and CFS demonstrate significant potential as therapeutic agents against H. pylori-triggered inflammation.
- This study provides the first evidence for the anti-inflammatory properties of L. crispatus EVs and CFS in the context of H. pylori infection.
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