ArticleBMC microbiology2023
The panda-derived Lactiplantibacillus plantarum BSG201683 improves LPS-induced intestinal inflammation and epithelial barrier disruption in vitro.
Article in BMC microbiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
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Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 8 citations in OpenAlex.
- Effect of probiotics on pregnancy outcomes in gestational diabetes: systematic review and meta-analysis.Archives of gynecology and obstetrics · 2024Pooled it
- Probiotic-Derived Antimicrobial Proteins and Peptides: Molecular Mechanisms, Clinical Applications, and Future Therapeutic Perspectives.Probiotics and antimicrobial proteins · 2026Review
- Protective Effects ofFoods (Basel, Switzerland) · 2026Article
- Gerobiotics: Exploring the Potential and Limitations of Repurposing Probiotics in Addressing Aging Hallmarks and Chronic Diseases.Probiotics and antimicrobial proteins · 2026Review
- Protective and therapeutic effects of Lactobacillus brevis PQ214320 and Bacillus subtilis PQ198038 Against experimental Trichinella Infection.PLoS neglected tropical diseases · 2025Article
- Indole‑3‑propionic acid alleviates intestinal epithelial cell injury via regulation of the TLR4/NF‑κB pathway to improve intestinal barrier function.Molecular medicine reports · 2024Article
- Probiotics: Shaping the gut immunological responses.World journal of gastroenterology · 2024Article
- Article
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Captive pandas are suffering from intestinal infection due to intestinal microbiota characterized by a high abundance of Enterobacteriaceae induced by long-term captivity. Probiotic supplements showed improvement in intestinal barrier function and inflammation. However, the effects of panda-derived probiotics on the intestinal epithelium and inflammation have not been elucidated. In the present study, lipopolysaccharide (LPS) impaired Caco-2 and RAW264.7 inflammatory models were applied to assess the protection of Lactiplantibacillus plantarum BSG201683 (L. plantarum G83) on barrier disruption and inflammation. The results showed that treatment with L. plantarum G83 significantly decreased the paracellular permeability to fluorescein isothiocyanate conjugated dextran (MW 4000, FITC-D4) after LPS induction. Meanwhile, L. plantarum G83 alleviated the reduction in tight junction (TJ) proteins and downregulated proinflammatory cytokines caused by LPS in Caco-2 cells. L. plantarum G83 also significantly decreased the expression and secretion of pro-inflammatory cytokines in LPS-induced RAW264.7 cells. In addition, the IL-10 increased in both Caco-2 and RAW264.7 cells after L. plantarum G83 treatment. The phagocytosis activity of RAW264.7 cells was significantly increased after L. plantarum G83 treatment. Toll-like receptor 4/ nuclear factor kappa-B (TLR4/NF-κB) signaling pathways were significantly down-regulated after L. plantarum G83 intervention, and the phosphorylation of NF-κB/p65 was consistent with this result. Our findings suggest that L. plantarum G83 improves intestinal inflammation and epithelial barrier disruption in vitro.
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