Lacticaseibacillus paracasei FL5 Inhibits Helicobacter pylori by Regulating Gastric Microbiota and NF-κB Signaling
Jialin Wang1, Pengyuan Pan1, Hailing Wang1
1College of Food Science and Engineering, Jilin Agricultural University, Changchun 130118, China.
Abstract:
Helicobacter pylori (H. pylori) infection causes severe gastropathies, and antibiotic resistance calls for alternative therapies. In this study, Lacticaseibacillus paracasei FL5 was the most potent H. pylori antagonist, showing excellent coaggregation (97.93%), high cell surface hydrophobicity (>50%), significant urease inhibition (77.58%), and a 22.00 mm inhibition zone. In vitro, its secreted metabolites induce bacterial lysis and inhibit urease. In vivo, FL5 and IFL5 (inactivated FL5) treated H. pylori-induced gastritis, reducing H. pylori colonization, regulating oxidative stress, and repairing the mucosal barrier. They also modulated gastric microbial homeostasis and attenuated inflammation via the TLR2/MyD88/NF-κB pathway (decreased TNF-α/IL-1β/IL-6/CXCL1, increased IL-10/IL-4 and IgG). Interestingly, IFL5 demonstrated superior efficacy to live FL5 in inhibiting TLR2/NF-κB signaling, highlighting the retained immunomodulatory activity of the heat-inactivated derivative. These findings establish L. paracasei FL5 as a promising multitarget therapeutic approach.
Insights
Lacticaseibacillus paracasei FL5 effectively combats H. pylori infection by inhibiting urease and reducing bacterial colonization. Its inactivated form shows enhanced immunomodulatory effects, offering a promising alternative therapy for gastritis.
Area of Science:
- Microbiology and Immunology
- Gastroenterology
- Probiotics and Gut Health
Background:
- Helicobacter pylori infection is a major cause of severe gastropathies.
- Increasing antibiotic resistance necessitates novel therapeutic strategies.
- Probiotics offer a potential alternative for managing H. pylori-associated conditions.
Purpose of the Study:
- To evaluate the efficacy of Lacticaseibacillus paracasei FL5 as an antagonist against H. pylori.
- To investigate the in vitro and in vivo therapeutic potential of L. paracasei FL5 and its inactivated derivative (IFL5).
- To elucidate the immunomodulatory mechanisms underlying the therapeutic effects.
Main Methods:
- In vitro assessment of L. paracasei FL5's antagonistic properties, including coaggregation, hydrophobicity, and urease inhibition.
- Analysis of secreted metabolites for bacterial lysis and urease inhibition.
- In vivo study using a mouse model of H. pylori-induced gastritis to evaluate FL5 and IFL5 effects on colonization, oxidative stress, mucosal repair, and immune response (TLR2/MyD88/NF-κB pathway).
Main Results:
- L. paracasei FL5 demonstrated potent H. pylori antagonism with high coaggregation (97.93%), hydrophobicity (>50%), and significant urease inhibition (77.58%).
- FL5 and IFL5 treatments reduced H. pylori colonization, regulated oxidative stress, and repaired the gastric mucosal barrier in vivo.
- IFL5 exhibited superior inhibition of TLR2/MyD88/NF-κB signaling compared to live FL5, indicating retained immunomodulatory activity.
Conclusions:
- Lacticaseibacillus paracasei FL5 is a potent H. pylori antagonist with significant therapeutic potential.
- Both live FL5 and its inactivated form (IFL5) effectively manage H. pylori-induced gastritis by modulating microbial homeostasis and immune responses.
- The retained immunomodulatory activity of inactivated FL5 highlights its promise as a stable and effective therapeutic agent.
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