Lactobacillus plantarum L15 Alleviates Colitis by Inhibiting LPS-Mediated NF-κB Activation and Ameliorates DSS-Induced Gut Microbiota Dysbiosis

Peng, Yu; Ke, Chuxin; Guo, Jiaxin; Zhang, Xiuling; Li, Bailiang

doi:10.3389/fimmu.2020.575173

Cited by 65 publications

(42 citation statements)

References 74 publications

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“…Upon ligand binding, MyD88-dependent signaling can result in the phosphorylation of NF-kB, a transcription factor that regulates the levels of IL-1b, IL-6, TNF-a, and several other inflammatory factors, in response to NLRP3 (53,54). Consistent with previous investigations (55,56), our study showed that Kae could inhibit the expression of inflammatory-associated mediators by dampening the activation of the LPS-TLR4-NF-kB signaling in mice with DSStriggered colitis.…”

Section: Discussionsupporting

confidence: 91%

Kaempferol Alleviates Murine Experimental Colitis by Restoring Gut Microbiota and Inhibiting the LPS-TLR4-NF-κB Axis

Yan

et al. 2021

Front. Immunol.

118

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Intestinal microbiota dysbiosis is an established characteristic of ulcerative colitis (UC). Regulating the gut microbiota is an attractive alternative UC treatment strategy, considering the potential adverse effects of synthetic drugs used to treat UC. Kaempferol (Kae) is an anti-inflammatory and antioxidant flavonoid derived from a variety of medicinal plants. In this study, we determined the efficacy and mechanism of action of Kae as an anti-UC agent in dextran sulfate sodium (DSS)-induced colitis mice. DSS challenge in a mouse model of UC led to weight loss, diarrhea accompanied by mucous and blood, histological abnormalities, and shortening of the colon, all of which were significantly alleviated by pretreatment with Kae. In addition, intestinal permeability was shown to improve using fluorescein isothiocyanate (FITC)–dextran administration. DSS-induced destruction of the intestinal barrier was also significantly prevented by Kae administration via increases in the levels of ZO-1, occludin, and claudin-1. Furthermore, Kae pretreatment decreased the levels of IL-1β, IL-6, and TNF-α and downregulated transcription of an array of inflammatory signaling molecules, while it increased IL-10 mRNA expression. Notably, Kae reshaped the intestinal microbiome by elevating the Firmicutes to Bacteroidetes ratio; increasing the linear discriminant analysis scores of beneficial bacteria, such as Prevotellaceae and Ruminococcaceae; and reducing the richness of Proteobacteria in DSS-challenged mice. There was also an evident shift in the profile of fecal metabolites in the Kae treatment group. Serum LPS levels and downstream TLR4-NF-κB signaling were downregulated by Kae supplementation. Moreover, fecal microbiota transplantation from Kae-treated mice to the DSS-induced mice confirmed the effects of Kae on modulating the gut microbiota to alleviate UC. Therefore, Kae may exert protective effects against colitis mice through regulating the gut microbiota and TLR4-related signaling pathways. This study demonstrates the anti-UC effects of Kae and its potential therapeutic mechanisms, and offers novel insights into the prevention of inflammatory diseases using natural products.

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Section: Discussionsupporting

confidence: 91%

Kaempferol Alleviates Murine Experimental Colitis by Restoring Gut Microbiota and Inhibiting the LPS-TLR4-NF-κB Axis

Yan

et al. 2021

Front. Immunol.

118

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“…In this experiment, although the difference was insignificant, the proinflammatory factors showed an upward trend after ETEC challenge, which indicated that ETEC increased intestinal inflammation in mice. Probiotics can reduce the inflammatory response by reducing the level of cytokines [12,34,35], which is also proven by our research. Although 6…”

Section: Discussionsupporting

confidence: 77%

“…Lactic acid bacteria, a kind of probiotic that exists in human and animal intestines, can enhance the immune system by inhibiting the expression of proinflammatory cytokines or promoting that of anti-inflammatory cytokines [ 10 , 11 ]. Lactobacillus plantarum is a major species of lactic acid bacteria, with a variety of probiotic characteristics, gastrointestinal transport tolerance, and anti-inflammatory properties [ 12 ]. Previous studies have shown that the supplementation of L. plantarum in the diet can promote the gastrointestinal health of weaned piglets [ 13 ] and improve the antioxidant status and growth performance of piglets [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

Lactobacillus plantarum and Lactobacillus brevis Alleviate Intestinal Inflammation and Microbial Disorder Induced by ETEC in a Murine Model

Han

Ding

et al. 2021

Oxidative Medicine and Cellular Longevity

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The purpose of this research is to explore the positive effects of Lactobacillus plantarum and Lactobacillus brevis on the tissue damage and microbial community in mice challenged by Enterotoxigenic Escherichia coli (ETEC). Twenty-four mice were divided into four groups randomly: the CON group, ETEC group, LP-ETEC group and LB-ETEC group. Our results demonstrated that, compared with the ETEC group, the LP-ETEC and LB-ETEC groups experienced less weight loss and morphological damage of the jejunum. We measured proinflammatory factors of colonic tissue and found that L. plantarum and L. brevis inhibited the expression of proinflammatory factors such as IL-β, TNF-α, and IL-6 and promoted that of the tight junction protein such as claudin-1, occludin, and ZO-1. Additionally, L. plantarum and L. brevis altered the impact of ETEC on the intestinal microbial community of mice, significantly increased the abundance of probiotics such as Lactobacillus, and reduced that of pathogenic bacteria such as Proteobacteria, Clostridia, Epsilonproteobacteria, and Helicobacter. Therefore, we believe that L. plantarum and L. brevis can stabilize the intestinal microbiota and inhibit the growth of pathogenic bacteria, thus protecting mice from the gut inflammation induced by ETEC.

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“…The relative mRNA levels of tight junction protein genes (claudin-1, occluding and ZO-1) and TLR4 signaling pathway related genes (TLR4, MYD88 and NF-κB) were detected by quantitative real-time polymerase chain reaction (qRT-PCR), and GAPDH gene was used as an internal reference gene. The primers used for qRT-PCR were described in previous studies [27]. Total RNA of the colon was extracted with RNAiso Plus ((Takara Biotechnology, Dalian, China) and quantified by using 2000C Ultra-micro UV spectrophotometer (Thermo Fisher Scientific Inc., Waltham, MA, USA).…”

Section: Real-time Quantitative Polymerase Chain Reaction (Qrt-pcr)mentioning

confidence: 99%

Alleviation Effects of Bifidobacterium animalis subsp. lactis XLTG11 on Dextran Sulfate Sodium-Induced Colitis in Mice

Wang

et al. 2021

Microorganisms

Self Cite

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Inflammatory bowel disease (IBD) is a chronic immune-related disease, which can occur through the dysfunction of the immune system caused by the imbalance of gut microbiota. Previous studies have reported the beneficial effects of Bifidobacterium on colitis, while the related mechanisms behind these effects have not been fully elucidated. The aim of our study is to investigate the alleviation effect of Bifidobacterium animalis subsp. lactis XLTG11 (B. lactis) on dextran sulfate sodium (DSS)-induced colitis and its potential mechanism. The results showed that B. lactis XLTG11 significantly decreased weight loss, disease activity index score, colon shortening, myeloperoxide activity, spleen weight, and colon tissue damage. Additionally, B. lactis XLTG11 significantly decreased the levels of pro-inflammatory cytokines and increased the level of anti-inflammatory cytokine. Meanwhile, high doses of B. lactis XLTG11 significantly up-regulated the expression of tight junction proteins and inhibited activation of Toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MYD88)/nuclear factor-κB (NF-κB) signaling pathway. Furthermore, B. lactis XLTG11 increased the gut microbiota diversity and modulated gut microbiota composition caused by DSS. Moreover, Spearman’s correlation analysis also found that several specific gut microbiota were significantly correlated with colitis-related indicators. These results demonstrated that B. lactis XLTG11 can alleviate DSS-induced colitis by inhibiting the activation of the TLR4/MYD88/NF-κB signaling pathway, regulating inflammatory cytokines, improving intestinal barrier function, and modulating the gut microbiota.

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Lactobacillus plantarum L15 Alleviates Colitis by Inhibiting LPS-Mediated NF-κB Activation and Ameliorates DSS-Induced Gut Microbiota Dysbiosis

Cited by 65 publications

References 74 publications

Kaempferol Alleviates Murine Experimental Colitis by Restoring Gut Microbiota and Inhibiting the LPS-TLR4-NF-κB Axis

Kaempferol Alleviates Murine Experimental Colitis by Restoring Gut Microbiota and Inhibiting the LPS-TLR4-NF-κB Axis

Lactobacillus plantarum and Lactobacillus brevis Alleviate Intestinal Inflammation and Microbial Disorder Induced by ETEC in a Murine Model

Alleviation Effects of Bifidobacterium animalis subsp. lactis XLTG11 on Dextran Sulfate Sodium-Induced Colitis in Mice

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