scholarly journals Intestinal Barrier Dysfunction, Bacterial Translocation and Inflammation: Deathly Triad in Sepsis

2021 ◽  
Author(s):  
Bercis Imge Ucar ◽  
Gulberk Ucar
Keyword(s):  
Bacterial Translocation ◽  
Current Knowledge ◽  
Intestinal Barrier ◽  
Intestinal Bacteria ◽  
Mucosal Barrier ◽  
High Morbidity ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction ◽  
Gut Mucosa ◽  
Sepsis Detection

Sepsis, as a complex entity, comprises multiple pathophysiological mechanisms which bring about high morbidity and mortality. The previous studies showed that the gastrointestinal tract is damaged during sepsis, and its main symptoms include increased permeability, bacterial translocation (BT), and malabsorption. BT is the invasion of indigenous intestinal bacteria via the gut mucosa to other tissues. It occurs in pathological conditions such as disruption of the intestine’s ecological balance and mucosal barrier permeability, immunosuppression, and oxidative stress through transcellular/paracellular pathways and initiate an excessive systemic inflammatory response. Thereby, recent clinical and preclinical studies focus on the association between sepsis and intestinal barrier dysfunction. This chapter overviews the current knowledge about the molecular basis of BT of the intestine, its role in the progress of sepsis, detection of BT, and actual therapeutic approaches.

The role of RAGE in the pathogenesis of intestinal barrier dysfunction after hemorrhagic shock

2006 ◽  
Vol 291 (4) ◽  
pp. G556-G565 ◽  
Author(s):  
Kathleen G. Raman ◽  
Penny L. Sappington ◽  
Runkuan Yang ◽  
Ryan M. Levy ◽  
Jose M. Prince ◽  
...  
Keyword(s):  
Hemorrhagic Shock ◽  
Bacterial Translocation ◽  
Intestinal Barrier ◽  
High Plasma ◽  
Mucosal Barrier ◽  
Barrier Dysfunction ◽  
Mesenteric Lymph Nodes ◽  
Mucosal Permeability ◽  
Intestinal Barrier Dysfunction ◽  
Soluble Rage

The receptor for advanced glycation end products (RAGE) has been implicated in the pathogenesis of numerous conditions associated with excessive inflammation. To determine whether RAGE-dependent signaling is important in the development of intestinal barrier dysfunction after hemorrhagic shock and resuscitation (HS/R), C57Bl/6, rage−/−, or congenic rage+/+ mice were subjected to HS/R (mean arterial pressure of 25 mmHg for 3 h) or a sham procedure. Twenty-four hours later, bacterial translocation to mesenteric lymph nodes and ileal mucosal permeability to FITC-labeled dextran were assessed. Additionally, samples of ileum were obtained for immunofluorescence microscopy, and plasma was collected for measuring IL-6 and IL-10 levels. HS/R in C57Bl/6 mice was associated with increased bacterial translocation, ileal mucosal hyperpermeability, and high circulating levels of IL-6. All of these effects were prevented when C57Bl/6 mice were treated with recombinant human soluble RAGE (sRAGE; the extracellular ligand-binding domain of RAGE). HS/R induced bacterial translocation, ileal mucosal hyperpermeability, and high plasma IL-6 levels in rage+/+ but not rage−/− mice. Circulating IL-10 levels were higher in rage−/− compared with rage+/+ mice. These results suggest that activation of RAGE-dependent signaling is a key factor leading to gut mucosal barrier dysfunction after HS/R.

Confirmation and Prevention of Intestinal Barrier Dysfunction and Bacterial Translocation Caused by Methotrexate

2006 ◽  
Vol 51 (9) ◽  
pp. 1549-1556 ◽  
Author(s):  
Desheng Song ◽  
Bin Shi ◽  
Hua Xue ◽  
Yousheng Li ◽  
Xiaodong Yang ◽  
...  
Keyword(s):  
Bacterial Translocation ◽  
Intestinal Barrier ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction

scholarly journals Obstructive jaundice promotes intestinal-barrier dysfunction and bacterial translocation: experimental study

2007 ◽  
Vol 1 (4) ◽  
pp. 444-448 ◽  
Author(s):  
Hesham Abdeldayem ◽  
Enas Ghoneim ◽  
Ahmad Ahmad-El Refaei ◽  
Ashraf Abou-Gabal
Keyword(s):  
Experimental Study ◽  
Obstructive Jaundice ◽  
Bacterial Translocation ◽  
Intestinal Barrier ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction

scholarly journals Prebiotic Inulin and Sodium Butyrate Attenuate Obesity-Induced Intestinal Barrier Dysfunction by Induction of Antimicrobial Peptides

2021 ◽  
Vol 12 ◽  
Author(s):  
Julia Beisner ◽  
Louisa Filipe Rosa ◽  
Valentina Kaden-Volynets ◽  
Iris Stolzer ◽  
Claudia Günther ◽  
...  
Keyword(s):  
Sodium Butyrate ◽  
Paneth Cell ◽  
Liver Steatosis ◽  
Intestinal Barrier ◽  
Histone Deacetylation ◽  
Mucosal Barrier ◽  
Barrier Dysfunction ◽  
Fermentation Products ◽  
Alcoholic Fatty Liver ◽  
Intestinal Barrier Dysfunction

Defects in the mucosal barrier have been associated with metabolic diseases such as obesity and non-alcoholic fatty liver disease (NAFLD). Mice fed a Western-style diet (WSD) develop obesity and are characterized by a diet-induced intestinal barrier dysfunction, bacterial endotoxin translocation and subsequent liver steatosis. To examine whether inulin or sodium butyrate could improve gut barrier dysfunction, C57BL/6 mice were fed a control diet or a WSD ± fructose supplemented with either 10% inulin or 5% sodium butyrate for 12 weeks respectively. Inulin and sodium butyrate attenuated hepatosteatitis in the WSD-induced obesity mouse model by reducing weight gain, liver weight, plasma and hepatic triglyceride level. Furthermore, supplementation with inulin or sodium butyrate induced expression of Paneth cell α-defensins and matrix metalloproteinase-7 (MMP7), which was impaired by the WSD and particularly the fructose-added WSD. Effects on antimicrobial peptide function in the ileum were accompanied by induction of β-defensin-1 and tight junction genes in the colon resulting in improved intestinal permeability and endotoxemia. Organoid culture of small intestinal crypts revealed that the short chain fatty acids (SCFA) butyrate, propionate and acetate, fermentation products of inulin, induce Paneth cell α-defensin expression in vitro, and that histone deacetylation and STAT3 might play a role in butyrate-mediated induction of α-defensins. In summary, inulin and sodium butyrate attenuate diet-induced barrier dysfunction and induce expression of Paneth cell antimicrobials. The administration of prebiotic fiber or sodium butyrate could be an interesting therapeutic approach to improve diet-induced obesity.

scholarly journals Hydrogen-Rich Saline Regulates Intestinal Barrier Dysfunction, Dysbiosis, and Bacterial Translocation in a Murine Model of Sepsis

Shock ◽  
2018 ◽  
Vol 50 (6) ◽  
pp. 640-647 ◽  
Author(s):  
Mitsunori Ikeda ◽  
Kentaro Shimizu ◽  
Hiroshi Ogura ◽  
Takashi Kurakawa ◽  
Eiji Umemoto ◽  
...  
Keyword(s):  
Bacterial Translocation ◽  
Murine Model ◽  
Intestinal Barrier ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction

scholarly journals Probiotics for Alleviating Alcoholic Liver Injury

2019 ◽  
Vol 2019 ◽  
pp. 1-8
Author(s):  
Zelin Gu ◽  
Yanlong Liu ◽  
Shumeng Hu ◽  
Ying You ◽  
Wancong Li ◽  
...  
Keyword(s):  
Liver Disease ◽  
Immune Responses ◽  
Alcoholic Liver Disease ◽  
Current Knowledge ◽  
Animal Experiments ◽  
Intestinal Flora ◽  
Intestinal Barrier ◽  
Intestinal Bacteria ◽  
Barrier Dysfunction ◽  
Mucosal Permeability

Many animal experiments and clinical trials showed that probiotics are effective for the treatment of alcoholic liver disease. Alcohol disrupts the composition of intestinal flora; probiotics modulate the gut microbiota and reverse alcohol-associated intestinal barrier dysfunction by decreasing intestinal mucosal permeability and preventing intestinal bacteria from translocating. Probiotics enhance immune responses and reduce the levels of alcohol-induced inflammatory cytokines and reactive oxygen species (ROS) production in the liver and intestine. Probiotics also increase fatty acid β-oxidation and reduce lipogenesis, combating alcohol-induced hepatic steatosis. In this review, we summarize the current knowledge regarding the mechanism of action of probiotics for reducing the effects of alcoholic liver disease.

scholarly journals Intestinal barrier dysfunction in severe burn injury

2019 ◽  
Vol 7 ◽  
Author(s):  
Wen He ◽  
Yu Wang ◽  
Pei Wang ◽  
Fengjun Wang
Keyword(s):  
Burn Injury ◽  
Current Knowledge ◽  
Intestinal Barrier ◽  
Multiple Organ ◽  
Intestinal Lumen ◽  
Burn Shock ◽  
Severe Burn ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction ◽  
Severe Burn Injury

Abstract Severe burn injury is often accompanied by intestinal barrier dysfunction, which is closely associated with post-burn shock, bacterial translocation, systemic inflammatory response syndrome, hypercatabolism, sepsis, multiple organ dysfunction syndrome, and other complications. The intestinal epithelium forms a physical barrier that separates the intestinal lumen from the internal milieu, in which the tight junction plays a principal role. It has been well documented that after severe burn injury, many factors such as stress, ischemia/hypoxia, proinflammatory cytokines, and endotoxins can induce intestinal barrier dysfunction via multiple signaling pathways. Recent advances have provided new insights into the mechanisms and the therapeutic strategies of intestinal epithelial barrier dysfunction associated with severe burn injury. In this review, we will describe the current knowledge of the mechanisms involved in intestinal barrier dysfunction in response to severe burn injury and the emerging therapies for treating intestinal barrier dysfunction following severe burn injury.

Intestinal barrier dysfunction in developing liver cirrhosis: An in vivo analysis of bacterial translocation

2007 ◽  
Vol 37 (1) ◽  
pp. 6-12 ◽  
Author(s):  
Pablo Palma ◽  
Nicolas Mihaljevic ◽  
Till Hasenberg ◽  
Michael Keese ◽  
Thomas A. Koeppel
Keyword(s):  
Liver Cirrhosis ◽  
Bacterial Translocation ◽  
Intestinal Barrier ◽  
Barrier Dysfunction ◽  
Intestinal Barrier Dysfunction ◽  
In Vivo Analysis

scholarly journals Soluble epoxide hydrolase is an endogenous regulator of obesity-induced intestinal barrier dysfunction and bacterial translocation

2020 ◽  
Vol 117 (15) ◽  
pp. 8431-8436 ◽  
Author(s):  
Yuxin Wang ◽  
Jun Yang ◽  
Weicang Wang ◽  
Katherine Z. Sanidad ◽  
Maris A. Cinelli ◽  
...  
Keyword(s):  
Bacterial Translocation ◽  
Epoxide Hydrolase ◽  
Intestinal Barrier ◽  
Soluble Epoxide Hydrolase ◽  
Gut Bacteria ◽  
Barrier Dysfunction ◽  
Genetic Ablation ◽  
Intestinal Barrier Dysfunction ◽  
Gut Leakage ◽  
Adipose Inflammation

Intestinal barrier dysfunction, which leads to translocation of bacteria or toxic bacterial products from the gut into bloodstream and results in systemic inflammation, is a key pathogenic factor in many human diseases. However, the molecular mechanisms leading to intestinal barrier defects are not well understood, and there are currently no available therapeutic approaches to target intestinal barrier function. Here we show that soluble epoxide hydrolase (sEH) is an endogenous regulator of obesity-induced intestinal barrier dysfunction. We find that sEH is overexpressed in the colons of obese mice. In addition, pharmacologic inhibition or genetic ablation of sEH abolishes obesity-induced gut leakage, translocation of endotoxin lipopolysaccharide or bacteria, and bacterial invasion-induced adipose inflammation. Furthermore, systematic treatment with sEH-produced lipid metabolites, dihydroxyeicosatrienoic acids, induces bacterial translocation and colonic inflammation in mice. The actions of sEH are mediated by gut bacteria-dependent mechanisms, since inhibition or genetic ablation of sEH fails to attenuate obesity-induced gut leakage and adipose inflammation in mice lacking gut bacteria. Overall, these results support that sEH is a potential therapeutic target for obesity-induced intestinal barrier dysfunction, and that sEH inhibitors, which have been evaluated in human clinical trials targeting other human disorders, could be promising agents for prevention and/or treatment.

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