Bifidobacterium adolescentis CGMCC 15058 alleviates liver injury, enhances the intestinal barrier and modifies the gut microbiota in d-galactosamine-treated rats

2018 ◽  
Vol 103 (1) ◽  
pp. 375-393 ◽  
Author(s):  
Yating Li ◽  
Longxian Lv ◽  
Jianzhong Ye ◽  
Daiqiong Fang ◽  
Ding Shi ◽  
...  
Keyword(s):  
Liver Injury ◽  
Gut Microbiota ◽  
Intestinal Barrier ◽  
Bifidobacterium Adolescentis

scholarly journals S16 * GUT MICROBIOTA, INTESTINAL BARRIER FUNCTION, ENDOTOXEMIA AND ALCOHOLIC LIVER INJURY

2013 ◽  
Vol 48 (suppl 1) ◽  
pp. i17-i17
Author(s):  
S. Barve ◽  
R. Rao ◽  
K. Chaudhry ◽  
G. Samak ◽  
R. Gangwar ◽  
...  
Keyword(s):  
Liver Injury ◽  
Gut Microbiota ◽  
Barrier Function ◽  
Intestinal Barrier ◽  
Intestinal Barrier Function ◽  
Alcoholic Liver Injury

scholarly journals Gut Microbiota Participates in Antithyroid Drug Induced Liver Injury Through the Lipopolysaccharide Related Signaling Pathway

2020 ◽  
Vol 11 ◽  
Author(s):  
Jiayu Sun ◽  
Fuya Zhao ◽  
Baiqiang Lin ◽  
Jing Feng ◽  
Xin Wu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Gut Microbiota ◽  
Antithyroid Drug ◽  
Intestinal Barrier ◽  
Antithyroid Drugs ◽  
Sprague Dawley ◽  
Cross Sectional ◽  
Comparison Results ◽  
Gut Microbiota Dysbiosis ◽  
Microbiota Structure

Background: Drugs can alter the gut microbiota structure, and gut microbiota dysbiosis in turn is correlated with drug side effects through the intestinal endotoxemia hypothesis. Whether antithyroid drugs (including methimazole and propylthiouracil) cause gut microbiota dysbiosis and whether the gut microbiota is correlated with antithyroid drugs induced liver injury is unknown.Methods: Initial Graves’ disease patients were randomly divided into the methimazole group (n = 20) and the propylthiouracil group (n = 20) and were followed up every 2 weeks; 50 healthy controls were also included. The structure and function of gut microbiota were compared from the cross sectional and longitudinal levels. The correlation between the gut microbiota and clinical parameters was also determined. In addition, Sprague-Dawley rats were randomly allotted into six groups, including four drug groups, which received daily doses of methimazole (1.5 mg/kg/day; 2.5 mg/kg/day) or propylthiouracil (7.5 mg/kg/day; 12.5 mg/kg/day) by oral gavage, and two control groups received the vehicle. In addition to the indexes mentioned above, intestinal barrier-related indexes were also performed.Results: Cross sectional and longitudinal comparison results from both clinical trials and animal studies indicate that antithyroid drugs altered gut microbiota structure; and the liver function related indexes all increased which correlated with gut microbiota. In addition, lipopolysaccharide-related pathways and the lipopolysaccharide concentration in feces and serum all increased after antithyroid drugs administration. These results consistent with the destroyed intestinal barrier in animal study after antithyroid drugs administration.Conclusion: We verified that antithyroid drugs altered gut microbiota structure and that the gut microbiota may in turn be correlated with antithyroid drugs-induced liver injury through the intestinal endotoxemia hypothesis.

scholarly journals Constipation induced gut microbiota dysbiosis exacerbates experimental autoimmune encephalomyelitis in C57BL/6 mice

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Xiuli Lin ◽  
Yingying Liu ◽  
Lili Ma ◽  
Xiaomeng Ma ◽  
Liping Shen ◽  
...  
Keyword(s):  
Experimental Autoimmune Encephalomyelitis ◽  
Gut Microbiota ◽  
Blood Brain Barrier ◽  
Intestinal Barrier ◽  
Brain Barrier ◽  
Autoimmune Encephalomyelitis ◽  
Gm Csf ◽  
Blood Brain ◽  
Gut Microbiota Dysbiosis ◽  
Experimental Autoimmune

Abstract Background Constipation is a common gastrointestinal dysfunction which has a potential impact on people's immune state and their quality of life. Here we investigated the effects of constipation on experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis (MS). Methods Constipation was induced by loperamide in female C57BL/6 mice. The alternations of gut microbiota, permeability of intestinal barrier and blood–brain barrier, and histopathology of colon were assessed after constipation induction. EAE was induced in the constipation mice. Fecal microbiota transplantation (FMT) was performed from constipation mice into microbiota-depleted mice. Clinical scores, histopathology of inflammation and demyelination, Treg/Th17 and Treg17/Teff17 imbalance both in the peripheral lymphatic organs and central nervous system, cytokines include TGF-β, GM-CSF, IL-10, IL-17A, IL-17F, IL-21, IL-22, and IL-23 in serum were assessed in different groups. Results Compared with the vehicle group, the constipation mice showed gut microbiota dysbiosis, colon inflammation and injury, and increased permeability of intestinal barrier and blood–brain barrier. We found that the clinical and pathological scores of the constipation EAE mice were severer than that of the EAE mice. Compared with the EAE mice, the constipation EAE mice showed reduced percentage of Treg and Treg17 cells, increased percentage of Th17 and Teff17 cells, and decreased ratio of Treg/Th17 and Treg17/Teff17 in the spleen, inguinal lymph nodes, brain, and spinal cord. Moreover, the serum levels of TGF-β, IL-10, and IL-21 were decreased while the GM-CSF, IL-17A, IL-17F, IL-22, and IL-23 were increased in the constipation EAE mice. In addition, these pathological processes could be transferred via their gut microbiota. Conclusions Our results verified that constipation induced gut microbiota dysbiosis exacerbated EAE via aggravating Treg/Th17 and Treg17/Teff17 imbalance and cytokines disturbance in C57BL/6 mice.

scholarly journals Insights into the Impact of Microbiota in the Treatment of NAFLD/NASH and Its Potential as a Biomarker for Prognosis and Diagnosis

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 145
Author(s):  
Julio Plaza-Díaz ◽  
Patricio Solis-Urra ◽  
Jerónimo Aragón-Vela ◽  
Fernando Rodríguez-Rodríguez ◽  
Jorge Olivares-Arancibia ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Fecal Microbiota Transplantation ◽  
Liver Steatosis ◽  
Intestinal Barrier ◽  
Fecal Microbiota ◽  
Current Treatment ◽  
Immune Defense ◽  
Alcoholic Fatty Liver ◽  
The Impact

Non-alcoholic fatty liver disease (NAFLD) is an increasing cause of chronic liver illness associated with obesity and metabolic disorders, such as hypertension, dyslipidemia, or type 2 diabetes mellitus. A more severe type of NAFLD, non-alcoholic steatohepatitis (NASH), is considered an ongoing global health threat and dramatically increases the risks of cirrhosis, liver failure, and hepatocellular carcinoma. Several reports have demonstrated that liver steatosis is associated with the elevation of certain clinical and biochemical markers but with low predictive potential. In addition, current imaging methods are inaccurate and inadequate for quantification of liver steatosis and do not distinguish clearly between the microvesicular and the macrovesicular types. On the other hand, an unhealthy status usually presents an altered gut microbiota, associated with the loss of its functions. Indeed, NAFLD pathophysiology has been linked to lower microbial diversity and a weakened intestinal barrier, exposing the host to bacterial components and stimulating pathways of immune defense and inflammation via toll-like receptor signaling. Moreover, this activation of inflammation in hepatocytes induces progression from simple steatosis to NASH. In the present review, we aim to: (a) summarize studies on both human and animals addressed to determine the impact of alterations in gut microbiota in NASH; (b) evaluate the potential role of such alterations as biomarkers for prognosis and diagnosis of this disorder; and (c) discuss the involvement of microbiota in the current treatment for NAFLD/NASH (i.e., bariatric surgery, physical exercise and lifestyle, diet, probiotics and prebiotics, and fecal microbiota transplantation).

scholarly journals The Influence of Gut Microbiota on the Cardiovascular System Under Conditions of Obesity and Chronic Stress

2021 ◽  
Vol 23 (5) ◽  
Author(s):  
Piotr Dubinski ◽  
Katarzyna Czarzasta ◽  
Agnieszka Cudnoch-Jedrzejewska
Keyword(s):  
Gut Microbiota ◽  
Cardiovascular System ◽  
Chronic Stress ◽  
Human Body ◽  
High Fat Diet ◽  
Intestinal Barrier ◽  
Microbial Composition ◽  
Enhanced Absorption ◽  
Bacterial Accumulation ◽  
Metabolic Endotoxemia

Abstract Purpose of Review Based on the available data, it can be assumed that microbiota is an integral part of the human body. The most heavily colonized area of the human body is the gut, with bacterial accumulation ranging from 101–103 cells/g in the upper intestine to 1011–1012 cells/g in the colon. However, colonization of the gut is not the same throughout, as it was shown that there are differences between the composition of the microbiota in the intestine lumen and in the proximity of the mucus layer. Recent Findings Gut microbiota gradient can be differentially regulated by factors such as obesity and chronic stress. In particular, a high fat diet influences the gut microbial composition. It was also found that chronic stress may cause the development of obesity and thus change the organization of the intestinal barrier. Recent research has shown the significant effect of intestinal microflora on cardiovascular function. Enhanced absorption of bacterial fragments, such as lipopolysaccharide (LPS), promotes the onset of “metabolic endotoxemia,” which could activate toll-like receptors, which mediates an inflammatory response and in severe cases could cause cardiovascular diseases. It is presumed that the intestinal microbiota, and especially its metabolites (LPS and trimethylamine N-oxide (TMAO)), may play an important role in the pathogenesis of arterial hypertension, atherosclerosis, and heart failure. Summary This review focuses on how gut microbiota can change the morphological and functional activity of the cardiovascular system in the course of obesity and in conditions of chronic stress.

Sign in / Sign up

Export Citation Format

Share Document