Juliana Paula Bruch-Bertani1,2, Carolina Uribe-Cruz1,2, Amanda Pasqualotto1,2, Larisse Longo1,2, Raquel Ayres1, Carolina Bortolin Beskow1,2, Afonso Luis Barth3, Daiana Lima-Morales3, Fábio Meurer4, Gabriel Tayguara Silveira Guerreiro1, Themis Reverbel da Silveira1,2, Mário Reis Álvares-da-Silva1,2,5, Valesca Dall'Alba1,2,6. 1. Experimental Laboratory of Hepatology and Gastroenterology, Hospital de Clínicas de Porto Alegre (HCPA), Porto Alegre, Brazil. 2. Post Graduate Program in Gastroenterology and Hepatology, Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, Brazil. 3. Research Laboratory on Bacterial Resistance (LABRESIS), Hospital de Clínicas de Porto Alegre (HCPA), Porto Alegre, Brazil. 4. Post Graduate Program in Sustainable Development of Aquaculture, Universidade Federal do Paraná, Campus de Palotina, Paraná, Brazil. 5. Department of Internal Medicine, Gastroenterology and Hepatology Unit. School of Medicine, UFRGS. Gastroenterology and Hepatology Division, HCPA, Porto Alegre, Brazil. 6. Department of Nutrition. School of Medicine, UFRGS. Nutrition Division. Hospital de Clínicas de Porto Alegre, UFRGS. Porto Alegre, Brazil.
Abstract
Objective: Alcoholic liver disease (ALD) is among the leading causes of death from liver disease. Among the factors involved in its pathogenesis are inflammation and increased intestinal permeability. The aim of this study was to assess the effect of Lactobacillus rhamnosus GG (LGG) on hepatic lipid accumulation, activation of inflammasomes, and gut permeability markers in experimental model of ALD with zebrafish. Methods: An experiment was conducted to assess the effective LGG dose capable of promoting intestinal colonization. Animals were divided into three groups (n = 64/group): ethanol group (E), ethanol + probiotic group (EP), and control group (C). Groups E and EP were exposed to 0.5% ethanol concentration for 28 days. At the end of this period, animals were euthanized, and livers were collected for Oil Red staining and assessment of the inflammasome system. Intestines were collected for evaluation of gut permeability markers. Results: The dose of 1.55 × 106 UFC LGG/fish/d promoted intestinal colonization. Group EP presented lower hepatic lipid accumulation, lower il-1β expression, and higher cldn15a expression when compared to group E.Conclusions: Supplementation with LGG was protective for hepatic steatosis in ALD model. In addition, LGG influenced the modulation of the inflammatory response and markers of gut permeability, improving the gut barrier structure.
Objective: Alcoholic liver disease (ALD) is among the leading causes of death from liver disease. Among the factors involved in its pathogenesis are inflammation and increased intestinal permeability. The aim of this study was to assess the effect of Lactobacillus rhamnosus GG (LGG) on hepatic lipid accumulation, activation of inflammasomes, and gut permeability markers in experimental model of ALD with zebrafish. Methods: An experiment was conducted to assess the effective LGG dose capable of promoting intestinal colonization. Animals were divided into three groups (n = 64/group): ethanol group (E), ethanol + probiotic group (EP), and control group (C). Groups E and EP were exposed to 0.5% ethanol concentration for 28 days. At the end of this period, animals were euthanized, and livers were collected for Oil Red staining and assessment of the inflammasome system. Intestines were collected for evaluation of gut permeability markers. Results: The dose of 1.55 × 106 UFC LGG/fish/d promoted intestinal colonization. Group EP presented lower hepatic lipid accumulation, lower il-1β expression, and higher cldn15a expression when compared to group E.Conclusions: Supplementation with LGG was protective for hepatic steatosis in ALD model. In addition, LGG influenced the modulation of the inflammatory response and markers of gut permeability, improving the gut barrier structure.