The panda-derived Lactiplantibacillus plantarum BSG201683 improves LPS-induced intestinal inflammation and epithelial barrier disruption in vitro

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...

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Main Authors: Yi Zhou, Ling Duan, Yan Zeng, Xu Song, Kangcheng Pan, Lili Niu, Yang Pu, Jiakun Li, Abdul Khalique, Jing Fang, Bo Jing, Dong Zeng, Bairong Shen, Xueqin Ni
Format: Article
Language:English
Published: BMC 2023-09-01
Series:BMC Microbiology
Subjects:
Online Access:https://doi.org/10.1186/s12866-023-02928-4
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author Yi Zhou
Ling Duan
Yan Zeng
Xu Song
Kangcheng Pan
Lili Niu
Yang Pu
Jiakun Li
Abdul Khalique
Jing Fang
Bo Jing
Dong Zeng
Bairong Shen
Xueqin Ni
author_facet Yi Zhou
Ling Duan
Yan Zeng
Xu Song
Kangcheng Pan
Lili Niu
Yang Pu
Jiakun Li
Abdul Khalique
Jing Fang
Bo Jing
Dong Zeng
Bairong Shen
Xueqin Ni
author_sort Yi Zhou
collection DOAJ
description 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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spelling doaj.art-a499137731de48fc92969944c3cc692a2023-11-19T12:33:06ZengBMCBMC Microbiology1471-21802023-09-0123111710.1186/s12866-023-02928-4The panda-derived Lactiplantibacillus plantarum BSG201683 improves LPS-induced intestinal inflammation and epithelial barrier disruption in vitroYi Zhou0Ling Duan1Yan Zeng2Xu Song3Kangcheng Pan4Lili Niu5Yang Pu6Jiakun Li7Abdul Khalique8Jing Fang9Bo Jing10Dong Zeng11Bairong Shen12Xueqin Ni13Animal Microecology Research Center, College of Veterinary Medicine, Sichuan Agricultural UniversityAnimal Feed Affairs of Sichuan Province, Sichuan Provincial Department of Agriculture and Rural AffairsAnimal Microecology Research Center, College of Veterinary Medicine, Sichuan Agricultural UniversityAnimal Microecology Research Center, College of Veterinary Medicine, Sichuan Agricultural UniversityAnimal Microecology Research Center, College of Veterinary Medicine, Sichuan Agricultural UniversityChengdu Wildlife InstituteChengdu Wildlife InstituteDepartment of Urology and Institutes for Systems Genetics, Frontiers Science Center for Disease-Related Molecular Network, West China Hospital, Sichuan UniversityAnimal Microecology Research Center, College of Veterinary Medicine, Sichuan Agricultural UniversityAnimal Microecology Research Center, College of Veterinary Medicine, Sichuan Agricultural UniversityAnimal Microecology Research Center, College of Veterinary Medicine, Sichuan Agricultural UniversityAnimal Microecology Research Center, College of Veterinary Medicine, Sichuan Agricultural UniversityDepartment of Urology and Institutes for Systems Genetics, Frontiers Science Center for Disease-Related Molecular Network, West China Hospital, Sichuan UniversityAnimal Microecology Research Center, College of Veterinary Medicine, Sichuan Agricultural UniversityAbstract 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.https://doi.org/10.1186/s12866-023-02928-4ProbioticLactobacillusInflammationPermeabilityTight junction
spellingShingle Yi Zhou
Ling Duan
Yan Zeng
Xu Song
Kangcheng Pan
Lili Niu
Yang Pu
Jiakun Li
Abdul Khalique
Jing Fang
Bo Jing
Dong Zeng
Bairong Shen
Xueqin Ni
The panda-derived Lactiplantibacillus plantarum BSG201683 improves LPS-induced intestinal inflammation and epithelial barrier disruption in vitro
BMC Microbiology
Probiotic
Lactobacillus
Inflammation
Permeability
Tight junction
title The panda-derived Lactiplantibacillus plantarum BSG201683 improves LPS-induced intestinal inflammation and epithelial barrier disruption in vitro
title_full The panda-derived Lactiplantibacillus plantarum BSG201683 improves LPS-induced intestinal inflammation and epithelial barrier disruption in vitro
title_fullStr The panda-derived Lactiplantibacillus plantarum BSG201683 improves LPS-induced intestinal inflammation and epithelial barrier disruption in vitro
title_full_unstemmed The panda-derived Lactiplantibacillus plantarum BSG201683 improves LPS-induced intestinal inflammation and epithelial barrier disruption in vitro
title_short The panda-derived Lactiplantibacillus plantarum BSG201683 improves LPS-induced intestinal inflammation and epithelial barrier disruption in vitro
title_sort panda derived lactiplantibacillus plantarum bsg201683 improves lps induced intestinal inflammation and epithelial barrier disruption in vitro
topic Probiotic
Lactobacillus
Inflammation
Permeability
Tight junction
url https://doi.org/10.1186/s12866-023-02928-4
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