Lacticaseibacillus paracasei FL5 demonstrated potent anti-H. pylori activity through multiple mechanisms including coaggregation, urease inhibition, and modulation of gastric microbiota and TLR2/MyD88/NF-κB signaling, with inactivated FL5 showing superior efficacy to live FL5 in inhibiting TLR2/NF-κB signaling.
Key Findings
Results
Lacticaseibacillus paracasei FL5 was identified as the most potent H. pylori antagonist among tested strains.
FL5 showed excellent coaggregation rate of 97.93% with H. pylori
Cell surface hydrophobicity exceeded 50%
Urease inhibition reached 77.58%
FL5 produced a 22.00 mm inhibition zone against H. pylori
Results
FL5 secreted metabolites induced bacterial lysis and inhibited urease activity in vitro.
The inhibitory effects were attributed to secreted metabolites rather than direct cell contact
Two distinct mechanisms were identified: bacterial lysis induction and urease inhibition
These in vitro findings supported the multi-target mechanism of FL5
Results
Both FL5 and inactivated FL5 (IFL5) reduced H. pylori colonization and treated H. pylori-induced gastritis in vivo.
In vivo treatment with FL5 and IFL5 reduced H. pylori colonization in gastric tissue
Both treatments regulated oxidative stress in H. pylori-infected animals
Both treatments repaired the mucosal barrier damaged by H. pylori infection
IFL5 refers to heat-inactivated FL5
Results
FL5 and IFL5 modulated gastric microbial homeostasis in H. pylori-infected animals.
Treatment with FL5 and IFL5 altered gastric microbiota composition
The modulation of gastric microbial homeostasis was observed in vivo
This finding suggests that the probiotic exerts effects partly through reshaping the gastric microbial community
Results
FL5 and IFL5 attenuated inflammation via the TLR2/MyD88/NF-κB signaling pathway.
Treatment decreased pro-inflammatory cytokines TNF-α, IL-1β, IL-6, and CXCL1
Treatment increased anti-inflammatory markers IL-10, IL-4, and IgG
The signaling pathway identified was TLR2/MyD88/NF-κB
Both live and inactivated forms demonstrated immunomodulatory activity
Results
Inactivated FL5 (IFL5) demonstrated superior efficacy compared to live FL5 in inhibiting TLR2/NF-κB signaling.
IFL5 showed greater inhibition of TLR2/NF-κB signaling than live FL5
This finding highlights the retained immunomodulatory activity of the heat-inactivated derivative
The superior performance of IFL5 in this pathway was described as an unexpected or noteworthy finding, noted with 'interestingly' by the authors
Wang J, Pan P, Wang H, Huang Y, Ren D, Jiang B. (2026). Lacticaseibacillus paracasei FL5 Inhibits Helicobacter pylori by Regulating Gastric Microbiota and NF-κB Signaling Pathway.. Journal of agricultural and food chemistry. https://doi.org/10.1021/acs.jafc.5c11621