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Beneficial Shifts in Gut Microbiota by Lacticaseibacillus rhamnosus R0011 and Lactobacillus helveticus R0052 in Alcoholic Hepatitis.

ABSTRACT: Gut microbiota performs indispensable functions in the pathophysiology of alcoholic hepatitis (AH). We investigated the effects of Lacticaseibacillus rhamnosus R0011 and Lactobacillus helveticus for gut microbial restoration toward eubiosis in patients with AH. A multicenter, double-blind, and randomized trial was conducted. Probiotics (n = 44) and placebo (n = 45) groups received, during 7 days, L. rhamnosus R0011/L. helveticus R0052 at 120 mg/day and placebo. All patients were hospitalized to ensure abstinence. Liver function, lipopolysaccharide level, and stool analysis were evaluated in patients before and after 7 days of treatment. At baseline, the dominant bacteria were Gram-negative in both groups which decreased after the probiotics treatment and exhibited a significant reduction in lipopolysaccharide level (p < 0.001). The probiotics ameliorated the Child-Pugh scores (p < 0.001). Furthermore, the probiotics group showed a decline in the levels of alanine aminotransferase and gamma-glutamyltranspeptidase (p < 0.05). The probiotics changed the gut microbial composition at various taxonomical levels. The proportion of Bacteroidetes (147%) was increased after 7 days of probiotics supplementation while Proteobacteria (30%) and Fusobacteria (0%) were decreased. Administration of L. rhamnosus R0011 and L. helveticus R0052 conceivably associated with restoration of gut microbiome in AH patients and improved AH by modulating the gut-liver axis.

SUBMITTER: Gupta H

PROVIDER: S-EPMC9319967 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Host intestinal epithelial cells (IEC) present at the gastrointestinal interface are exposed to pathogenic and non-pathogenic bacteria and their products. Certain probiotic lactic acid bacteria (LAB) have been associated with a range of host-immune modulatory activities including down-regulation of pro-inflammatory gene expression and cytokine production by IEC, with growing evidence suggesting that these bacteria secrete bioactive molecules with immunomodulatory activity. The aim of this study was to determine whether two lactobacilli with immunomodulatory activity [Lactobacillus rhamnosus R0011 (Lr) and Lactobacillus helveticus R0389 (Lh)], produce soluble mediators able to influence IEC responses to Pattern Recognition Receptor (PRR) ligands and pro-inflammatory cytokines [Tumor Necrosis Factor ? (TNF?), Interleukin-1? (IL-1?)], signals inducing IEC chemokine production during infection. To this end, the effects of cell-free supernatants (CFS) from Lr and Lh on IEC production of the pro-inflammatory chemokines interleukin (IL)-8 and cytokine-induced neutrophil chemoattractant 1 (CINC-1) induced by a range of host- or pathogen-derived pro-inflammatory stimuli were determined, and the impact on human HT-29 IEC and a primary IEC line (rat IEC-6) was compared. The Lr-CFS and Lh-CFS did not significantly modulate basal IL-8 production from HT-29 IECs or CINC-1 production from IEC-6 cells. However, both Lr-CFS and Lh-CFS significantly down-regulated IL-8 production from HT-29 IECs challenged with varied PRR ligands. Lr-CFS and Lh-CFS had differential effects on PRR-induced CINC-1 production by rat IEC-6 IECs, with no significant down-regulation of CINC-1 observed from IEC-6 IECs cultured with Lh-CFS. Further analysis of the Lr-CFS revealed down-regulation of IL-8 production induced by the pro-inflammatory cytokines IL-1? and TNF? Preliminary characterization of the bioactive constituent(s) of the Lr-CFS indicates that it is resistant to treatment with DNase, RNase, and an acidic protease, but is sensitive to alterations in pH. Taken together, these results indicate that these lactobacilli secrete bioactive molecules of low molecular weight that may modulate host innate immune activity through interactions with IEC.

Project description:BackgroundAlcoholic hepatitis (AH) is associated with gut dysbiosis. Comparative gut microbial profiles of acute alcoholic pancreatitis (AAP) and acute biliary disease (ABD) are not demonstrated. We aimed to compare gut microbiota of AH, AAP, and ABD patients with each other and with their respective healthy controls (HCs).MethodsFrom December 2016 to September 2017, consecutive patients with AH, AAP, and ABD (acute cholecystitis, acute biliary pancreatitis, and choledocholithiasis with cholangitis) were included in the study. Qualitative and functional stool microbiota comparative analysis was performed between groups, with AH as the reference comparator.ResultsOf 3564, 882, and 224 patients with liver disease, pancreatic disease, and biliary disease, respectively, after exclusion, 29 patients with AH and 7 patients each with AAP and ABD and their corresponding HCs were included in the study analysis. The alpha diversity between patients with AH and AAP was found to be significantly different. Significant relative abundance (RA) of Acinetobacter and Moraxella was noted among patients with AAP. Enterobacter, Atopobium, Synergistia, and Devosia were significantly higher in patients with ABD compared to patients with AH, in whom Faecalibacterium and Megamonas were higher. Functional pathways associated with carbohydrate metabolism, phenylpropanoid biosynthesis, and ethylbenzene degradation were significantly higher in AAP when compared to AH. Fatty acid and inositol phosphate metabolism and dioxin degradation were significantly upregulated in patients with ABD while lipid and fatty acid biosynthetic pathways and pathways associated with immune processes were upregulated in patients with AH.ConclusionsDifferential gut dysbiosis is evident in both patients with AH, AAP, and ABD and also in comparison to HCs. The differential microbiota among patients with AH and AAP maybe important in promotion and progression of liver or pancreatic disease among alcohol users and may be a potential therapeutic target, which needs to be confirmed in larger multicenter studies.

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Beneficial Shifts in Gut Microbiota by Lacticaseibacillus rhamnosus R0011 and Lactobacillus helveticus R0052 in Alcoholic Hepatitis.

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