Dietary Supplements

Lacticaseibacillus paracasei FL5 Inhibits Helicobacter pylori by Regulating Gastric Microbiota and NF-κB Signaling Pathway.

TL;DR

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

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

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

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

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

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

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

Have a question about this study?

Citation

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