Dataset Information

Simultaneous Amelioratation of Colitis and Liver Injury in Mice by Bifidobacterium longum LC67 and Lactobacillus plantarum LC27.

ABSTRACT: Disturbances in the gut microbiota composition are associated with chronic inflammatory diseases of the intestine and the liver. In a preliminary study, Lactobacillus plantarum LC27 and Bifidobacterium longum LC67 could inhibit Escherichia coli growth and lipopolysaccharide-induced NF-κB activation linked to gut inflammation. Here, we investigated their effects on 2,4,6-trinitrobenzesulfonic acid (TNBS)-induced colitis and liver damage in mice. First, oral administration of LC27 or LC67 (1 × 109 CFU/mouse) inhibited TNBS-induced colon shortening [F(5,30) = 100.66, P < 0.05] and myeloperoxidase activity [F(5,30) = 56.48, P < 0.05]. These probiotics restored TNBS-induced disturbance of gut microbiota, leading to the suppression of Proteobacteria to Bacteroidetes ratio and fecal and blood lipopolysaccharide levels. Second, LC27 and LC67 inhibited TNBS-induced NF-κB activation, reversed TNBS-suppressed tight junction protein expression, and restored Th17/Treg balance. Also, treatment with LC27 or LC67 significantly decreased TNBS-induced alanine transaminase [ALT, F(5,30) = 3.50, P < 0.05] and aspartate transaminase [AST, F(5,30) = 12.81, P < 0.05] levels in the blood, as well as t-butylhydroperoxide-induced ALT and AST levels. Finally, the mixture of LC27 and LC67 (0.5 × 109 CFU/mouse, respectively) synergistically attenuated TNBS- or t-butylhydroperoxide-induced colitis and liver damage. The capability of LC27 and LC67 to reverse TNBS-mediated microbiota shift and damage signals suggests that these probiotics may synergistically attenuate colitis and liver injury by alleviating gut microbiota imbalance.

SUBMITTER: Jang SE

PROVIDER: S-EPMC5951891 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Simultaneous Amelioratation of Colitis and Liver Injury in Mice by Bifidobacterium longum LC67 and Lactobacillus plantarum LC27.

Jang Se-Eun SE Jeong Jin-Ju JJ Kim Jeon-Kyung JK Han Myung Joo MJ Kim Dong-Hyun DH

Scientific reports 20180514 1

Disturbances in the gut microbiota composition are associated with chronic inflammatory diseases of the intestine and the liver. In a preliminary study, Lactobacillus plantarum LC27 and Bifidobacterium longum LC67 could inhibit Escherichia coli growth and lipopolysaccharide-induced NF-κB activation linked to gut inflammation. Here, we investigated their effects on 2,4,6-trinitrobenzesulfonic acid (TNBS)-induced colitis and liver damage in mice. First, oral administration of LC27 or LC67 (1 × 10< ...[more]

PMID: 29760423

Similar Datasets

Project description:Neuropsychiatric disorders including Alzheimer's disease (AD) may cause gut inflammation and dysbiosis. Gut inflammation-suppressing probiotics alleviate neuropsychiatric disorders. Herein, to understand whether anti-inflammatory probiotics Lactobacillus mucosae NK41 and Bifidobacterium longum NK46, which suppressed tumor necrosis factor (TNF)-α expression in lipopolysaccharide (LPS)-stimulated macrophages, could alleviate cognitive impairment, we first examined their effects on cognitive function, gut inflammation, and gut microbiota composition in 5xFAD-transgenic mice. Oral administration of NK41 or NK46 decreased cognitive impairment-like behaviors, hippocampal amyloid-β (Aβ), TNF-α and interleukin (IL)-1β expression, hippocampal NF-κB+Iba1+ cell population, and Aβ accumulation, while hippocampal brain-derived neurotropic factor (BDNF) and IL-10 expression and BDNF+NeuN+ cell population increased. They also decreased TNF-α and IL-1β expression and NF-κB+CD11c+ cell population in the colon. They also reduced fecal and blood LPS levels and gut Proteobacteria and Verrucomicrobia populations (including Akkkermansiaceae), which are positively associated with hippocampal TNF-α and fecal LPS levels and negatively correlated with hippocampal BDNF level. However, they increased Odoribactericeae, which positively correlated with BDNF expression level and TNF-α to IL-10 expression ratio. The combination of NK41 and NK46 (4:1, NKc), which potently inhibited TNF-α expression in LPS-stimulated macrophages, additively alleviated cognitive impairment-like behaviors in 5xFAD-transgenic or aged mice. NKc increased hippocampal BDNF+NeuN+ cell population and BDNF expression in 5xFAD-transgenic or aged mice, while hippocampal TNF-α and IL-1β expression decreased. NKc also decreased TNF-α and IL-1β expression in the colon and LPS levels in the blood and feces. These findings suggest that gut bacteria and its product LPS may be closely connected with occurrence of cognitive impairment and neuroinflammation and the combination of NK41 and NK46 can additively alleviate cognitive impairment and neuroinflammation by inducing NF-κB-suppressed BDNF expression and suppressing LPS-producing gut bacteria.

Project description:Gut lactobacilli and bifidobacteria on the immune homeostasis. Therefore, to understand the mechanism in vivo, we selected human fecal Lactobacillus rhamnosus NK210 and Bifidobacterium longum NK219, which strongly suppressed the IFN-γ to IL-10 expression (IIE) ratio in lipopolysaccharide-stimulated macrophages. Thereafter, we examined their effects on the endotoxin, antibiotics, or antitumor drug-stimulated immune imbalance in mice. Intraperitoneal injection of lipopolysaccharide and oral gavage of ampicillin increased IFN-γ and TNF-α expression in the spleen, colon, and hippocampus, while IL-10 expression decreased. However, intraperitoneal injection of cyclophosphamide suppressed IFN-γ, TNF-α, and IL-10 expression. LPS exposure induced splenic natural killer cell cytotoxicity against YAC-1 cells (sNK-C) and peritoneal macrophage phagocytosis against Candida albicans (pMA-P) activities, while cyclophosphamide and ampicillin treatments suppressed sNK-C and pMA-P activities. However, LPS, ampicillin, cyclophosphamide all increased IIE and TNF-α to IL-10 expression (TIE) ratios. Oral administration of NK210 and/or NK219 significantly reduced LPS-induced sNK-C, pMA-P, and IFN-γ expression, while cyclophosphamide- or ampicillin-suppressed sNK-C and pMA-P activities, cyclophosphamide-suppressed IFN-γ, TNF-α, and IL-10 expression, and ampicillin-suppressed IL-10 expression increased. Nevertheless, they suppressed LPS-, ampicillin-, or cyclophosphamide-induced IIE and TIE ratios, cognitive impairment, and gut dysbiosis. In particular, NK219, but not NK210, increased the IIE expression ratio in vitro and in vivo, and enhanced sNK-C and pMA-P activities in normal control mice, while cognitive function and gut microbiota composition were not significantly affected. These findings suggest that NK210, Lactobacillus sp, and NK219, Bifidobacterium additively or synergistically alleviate gut dysbiosis, inflammation, and cognitive impairment with immune imbalance by controlling IIE and TIE ratios.

Project description:Yak yogurt is a type of naturally fermented dairy product prepared by herdsmen in the Qinghai-Tibet Plateau, which is rich in microorganisms. In this study, a strain of Lactobacillus plantarum was isolated and identified from yak yogurt in Hongyuan, Sichuan Province and named Lactobacillus plantarum HFY05 (LP-HFY05). LP-HFY05 was compared with a common commercial strain of Lactobacillus delbrueckii subsp. bulgaricus (LDSB). LP-HFY05 showed better anti-artificial gastric acid and bile salt effects than LDSB in in vitro experiments, indicating its potential as a probiotic. In animal experiments, long-term alcohol gavage induced alcoholic liver injury. LP-HFY05 effectively reduced the liver index of mice with liver injury, downregulated the levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, triglyceride, total cholesterol, blood urea nitrogen, nitric oxide, and MDA and upregulated the levels of albumin, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase in the serum of liver-injured mice. LP-HFY05 also reduced the levels of interleukin (IL)-6, IL-12, tumor necrosis factor-alpha, and interferon-gamma in the serum of liver-injured mice. The pathological observations showed that LP-HFY05 reduced the damage to liver cells caused by alcohol. Quantitative polymerase chain reaction and Western blot assays further showed that LP-HFY05 upregulated neuronal nitric oxide synthase, endothelial nitric oxide synthase, manganese-SOD, cuprozinc-SOD, CAT, and inhibitor of κB-α mRNA and protein expression and downregulated the expression of nuclear factor-κB-p65 and inducible nitric oxide synthase in the livers of liver-injured mice. A fecal analysis revealed that LP-HFY05 regulated the microbial content in the intestinal tract of mice with liver injury, increased the content of beneficial bacteria, including Bacteroides, Bifidobacterium, and Lactobacillus and reduced the content of harmful bacteria, including Firmicutes, Actinobacteria, Proteobacteria, and Enterobacteriaceae, thus, regulating intestinal microorganisms to protect against liver injury. The effect of LP-HFY05 on liver-injured mice was better than that of LDSB, and the effect was similar to that of silymarin. LP-HFY05 is a high-quality microbial strain with a liver protective effect on experimental mice with alcoholic liver injury.

Dataset Information

Simultaneous Amelioratation of Colitis and Liver Injury in Mice by Bifidobacterium longum LC67 and Lactobacillus plantarum LC27.

Publications

Simultaneous Amelioratation of Colitis and Liver Injury in Mice by Bifidobacterium longum LC67 and Lactobacillus plantarum LC27.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets