Lactobacillus rhamnosus GG supernatant promotes intestinal barrier function, balances T reg and T H 17 cells and ameliorates hepatic injury in a mouse model of chronic-binge alcohol feeding

Chen, Ruicong; Xu, Lei; Du, Shanjie; Huang, Sisi; Wu, Huizi; Dong, Jiajia; Huang, Jianrong; Wang, Xiaodong; Feng, Wenke; Chen, Yongping

doi:10.1016/j.toxlet.2015.11.019

Cited by 93 publications

(50 citation statements)

References 35 publications

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“…Many studies have reported the protective effects of LCS against gut barrier injury caused by chemicals, such as alcohol, dextran sodium sulfate and hydrogen peroxide3536373839. However, little is known about the roles of LCS on pathogen-induced intestinal barrier injury.…”

Section: Resultsmentioning

confidence: 99%

Lactobacillus rhamnosus GG supernatant enhance neonatal resistance to systemic Escherichia coli K1 infection by accelerating development of intestinal defense

Zeng

Puthiyakunnon

et al. 2017

Sci Rep

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The objective of this study was to determine whether Lactobacillus rhamnosus GG culture supernatant (LCS) has a preventive effect against gut-derived systemic neonatal Escherichia coli (E. coli) K1 infection. The preventive effects were evaluated in human colonic carcinoma cell line Caco-2 and neonatal rat models. Our in vitro results showed that LCS could block adhesion, invasion and translocation of E. coli K1 to Caco-2 monolayer via up-regulating mucin production and maintaining intestinal integrity. In vivo experiments revealed that pre-treatment with LCS significantly decrease susceptibility of neonatal rats to oral E. coli K1 infection as reflected by reduced bacterial intestinal colonization, translocation, dissemination and systemic infections. Further, we found that LCS treated neonatal rats have higher intestinal expressions of Ki67, MUC2, ZO-1, IgA, mucin and lower barrier permeability than those in untreated rats. These results indicated that LCS could enhance neonatal resistance to systemic E. coli K1 infection via promoting maturation of neonatal intestinal defense. In conclusions, our findings suggested that LCS has a prophylactic effect against systemic E. coli K1 infection in neonates. Future studies aimed at identifying the specific active ingredients in LCS will be helpful in developing effective pharmacological strategies for preventing neonatal E. coli K1 infection.

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Section: Resultsmentioning

confidence: 99%

Lactobacillus rhamnosus GG supernatant enhance neonatal resistance to systemic Escherichia coli K1 infection by accelerating development of intestinal defense

Zeng

Puthiyakunnon

et al. 2017

Sci Rep

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“…Inhibition of hsp90 by 17-dimethylamino-ethylamino-17-demethoxygeldanamycin ameliorated the steatosis and liver inflammation induced by chronic-plus-binge ethanol feeding, which suggests that hsp90 is a promising therapeutic target for the treatment of ALD 96 . More recently, the chronic-plus-binge ethanol feeding model has also been used to test the therapeutic potential of many drugs/compounds, including a CB2 agonist 62 , betulin (a triterpene from the bark of Betula platyphylla Suk) 97 , luteolin (a flavonoid) 98 , Lactobacillus rhamnosus GG 99 , Korean Red Ginseng 100 , glycycoumarin (a representative coumarin from traditional Chinese Medicine licorice) 101 , flaxseed oil enriched in α-linolenic acid (a plant-derived n-3 polyunsaturated fatty acid) 102 , thymoquinone (a biologically active compound isolated from the seeds of Nigella sativa L.) 103 , and β-caryophyllene (BCP: a plant-derived FDA-approved food additive with anti-inflammatory properties) 104 . The data from these studies revealed that treatment with all of these components ameliorated the chronic-plus-binge alcohol-induced liver inflammation and steatosis in mice.…”

Section: Application Of Chronic-plus-binge Ethanol Model In Testing Tmentioning

confidence: 99%

Animal Models of Alcoholic Liver Disease: Pathogenesis and Clinical Relevance

Gao

Bertola

et al. 2017

gene expr

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Alcoholic liver disease (ALD), a leading cause of chronic liver injury worldwide, comprises a range of disorders including simple steatosis, steatohepatitis, cirrhosis, and hepatocellular carcinoma. Over the last five decades, many animal models that have been useful for the study of ALD pathogenesis have been developed. Recently, a chronic-plus-binge ethanol feeding model was reported. This model induces significant steatosis, hepatic neutrophil infiltration, and liver injury. A clinically relevant model of high-fat diet feeding plus binge ethanol was also developed, which highlights the risk of excessive binge drinking in obese/overweight individuals. All of these models recapitulate some features of the different stages of ALD and have been widely used by many investigators to study the pathogenesis of ALD and test therapeutic drugs/components. However, these models are somewhat variable, depending on mouse genetic background, ethanol dose, and animal facility environment. This review focuses on these models and discusses these variations and some methods to improve the feeding protocol. The pathogenesis, clinical relevance, and translational studies of these models are also discussed.

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“…139 Lactobacillus GG supplementation in mice has been shown to increase intestinal tight junction expression, prevent gut leakiness, balance Treg and T-helper (Th) 17 cells, and attenuate hepatic TNF-α production as well as oxidative stress. 72,141–143 Notably, the beneficial effects of probiotics are achieved not only by live bacteria, but also by heat-inactivated bacteria or bacteria culture supernatant. 144 Importantly, a study employing 16S ribosome RNA sequencing revealed that Lactobacillus GG not only reduced bacterial overgrowth in alcohol-fed mice, but also prevented alcohol-induced expansion of the Proteobacteria and Actinobacteria phyla, which implicates the capacity of Lactobacillus GG in orchestrating gut microbiota symbiosis.…”

Section: Targeting the Leaking Gut To Treat Aldmentioning

confidence: 99%

Targeting the gut barrier for the treatment of alcoholic liver disease

Zhou

Zhong

2017

Liver Research

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Alcohol consumption remains one of the predominant causes of liver disease and liver-related death worldwide. Intriguingly, dysregulation of the gut barrier is a key factor promoting the pathogenesis of alcoholic liver disease (ALD). A functional gut barrier, which consists of a mucus layer, an intact epithelial monolayer and mucosal immune cells, supports nutrient absorption and prevents bacterial penetration. Compromised gut barrier function is associated with the progression of ALD. Indeed, alcohol consumption disrupts the gut barrier, increases gut permeability, and induces bacterial translocation both in ALD patients and in experimental models with ALD. Moreover, alcohol consumption also causes enteric dysbiosis with both numerical and proportional perturbations. Here, we review and discuss mechanisms of alcohol-induced gut barrier dysfunction to better understand the contribution of the gut-liver axis to the pathogenesis of ALD. Unfortunately, there is no effectual Food and Drug Administration-approved treatment for any stage of ALD. Therefore, we conclude with a discussion of potential strategies aimed at restoring the gut barrier in ALD. The principle behind antibiotics, prebiotics, probiotics and fecal microbiota transplants is to restore microbial symbiosis and subsequently gut barrier function. Nutrient-based treatments, such as dietary supplementation with zinc, niacin or fatty acids, have been shown to regulate tight junction expression, reduce intestinal inflammation, and prevent endotoxemia as well as liver injury caused by alcohol in experimental settings. Interestingly, saturated fatty acids may also directly control the gut microbiome. In summary, clinical and experimental studies highlight the significance and efficacy of the gut barrier in treating ALD.

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Lactobacillus rhamnosus GG supernatant promotes intestinal barrier function, balances T reg and T H 17 cells and ameliorates hepatic injury in a mouse model of chronic-binge alcohol feeding

Cited by 93 publications

References 35 publications

Lactobacillus rhamnosus GG supernatant enhance neonatal resistance to systemic Escherichia coli K1 infection by accelerating development of intestinal defense

Lactobacillus rhamnosus GG supernatant enhance neonatal resistance to systemic Escherichia coli K1 infection by accelerating development of intestinal defense

Animal Models of Alcoholic Liver Disease: Pathogenesis and Clinical Relevance

Targeting the gut barrier for the treatment of alcoholic liver disease

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