Increased Intestinal Marker Absorption Due to Regional Permeability Changes and Decreased Intestinal Transit during Sepsis in the Rat

Wang, Q.; Pantzar, N.; Jeppsson, Bengt; Weström, Björn; Karlsson, Börje W.

doi:10.3109/00365529409094877

Cited by 25 publications

(18 citation statements)

References 29 publications

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“…LPS clearly damages the functional intestinal barrier, which results in an increase of mucosal permeability, and this is considered to be a major promoter of bacterial translocation (BT) [36]. Intraperitoneal injection of LPS could mimic infection by increasing gut paracellular permeability and inducing BT [37–39]. Gut paracellular permeability was significantly higher at 6 h after LPS injection [39].…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Fas and FasL Is Associated with Infectious Complications and Severity of Experimental Severe Acute Pancreatitis by Promoting Apoptosis of Lymphocytes

et al. 2014

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This study investigated the relationship of Fas and Fas ligand (FasL) expression and apoptosis of lymphocytes in relation to the pathogenic immune response and infectious complications observed in experimental severe acute pancreatitis in mice. Forty male Balb/c mice were randomly divided into control, mild (MAP), and severe acute pancreatitis (SAP) groups. Overexpression of Fas/FasL messenger ribonucleic acid (mRNA) and protein was observed in spleen-derived lymphocytes in SAP (p < 0.01). Apoptosis of these resulted in a depletion of circulating lymphocytes in this group (p < 0.05). A further significant change in the SAP group with infectious complications was observed. A positive relationship was found between the Fas/FasL expression and lymphocyte apoptosis, and negative relationships were observed between Fas/FasL expression and CD4+ and CD19+ lymphocytes and the CD4+/CD8+ ratio in SAP mice (p < 0.01). The results suggest that the overexpression of Fas/FasL is associated with infectious complications and severity of experimental severe acute pancreatitis by promoting apoptosis of lymphocytes.

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Section: Discussionmentioning

confidence: 99%

Overexpression of Fas and FasL Is Associated with Infectious Complications and Severity of Experimental Severe Acute Pancreatitis by Promoting Apoptosis of Lymphocytes

et al. 2014

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“…Leuprolide-treated Conv.R and Col. GF mice displayed higher serum endotoxin levels as compared with those treated with vehicle, confirming that sex steroid deprivation increases gut permeability. To further explore the effects of sex steroid withdrawal on gut permeability, Conv.R ovx and shamoperated mice were gavaged with FITC-dextran 4 weeks after surgery, and 4 hours later, the serum levels of FITC-dextran -an index of gut permeability -were measured (62). Ovx mice had higher serum levels of FITC-dextran than sham-operated mice ( Figure 4F), altogether showing that the intestinal barrier permeability is compromised following sex steroid depletion.…”

Section: Resultsmentioning

confidence: 99%

Sex steroid deficiency–associated bone loss is microbiota dependent and prevented by probiotics

Li¹,

Chassaing²,

Tyagi³

et al. 2016

Journal of Clinical Investigation

480

610

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“…Previous data, both in animals and humans, have already described increased gut permeability after the injection of viable E. coli 3 or after a single administration of E. coli endotoxin. 2 A failure of the intestinal barrier, which results in an increase of mucosal permeability, has been hypothesized to be a major promoter of BT; 28 however, the mechanisms underlying the process of BT are poorly defined. Possible routes for transmucosal passage of bacteria include both transcellular and paracellular pathways.…”

Section: Bacterial Translocationmentioning

confidence: 99%

“…The impairment of the gastrointestinal barrier function with massive bacterial translocation (BT) occurs during sepsis, both in human and in animal models. [1][2][3][4][5] In these circumstances, bacteria and their lysis products, such as lipopolysaccharide (LPS), gain access to portal and systemic circulations, producing critical deleterious effects. Sepsis is the most common cause of death for hospitalized patients.…”

Section: Sepsis Is Associated With Bacterial Translocation (Bt)mentioning

confidence: 99%

Myosin Light Chain Kinase Is Involved in Lipopolysaccharide-Induced Disruption of Colonic Epithelial Barrier and Bacterial Translocation in Rats

Moriez

Salvador–Cartier

Théodorou

et al. 2005

The American Journal of Pathology

128

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Sepsis is associated with bacterial translocation (BT)and changes in colonic paracellular permeability (CPP), but the link between these effects is unknown. The present study aimed to identify whether changes in CPP after lipopolysaccharide (LPS) administration triggers BT, colonic inflammation, visceral pain, and sickness behavior and to evaluate the role of myosin light chain kinase (MLCK) in colonocyte cytoskeleton contraction. Rats received the MLCK inhibitor ML-7 alone or combined with LPS. CPP was measured for 6 hours after administration. Visceral pain, food intake, BT, electron microscopy of tight junctions of colonocytes, cytokine levels, and Western blotting of phosphorylated MLC from colonic mucosa were assessed in a time range of 0 to 3 hours after treatment. Sepsis increased CPP at 0 to 6 hours after LPS and associated with tight junction morphological changes, increased MLC phosphorylation, and mucosal release of proinflammatory cytokines. Massive BT, visceral hyperalgesia, and reduced food intake were also observed. Addition of ML-7 prevented all LPSinduced effects, except for changes in food intake. In conclusion, LPS-mediated effects on CPP include gut inflammation, BT, and visceral hyperalgesia. Inhibition of MLCK-dependent colonocyte cytoskeleton contraction by ML-7 prevents the LPS-induced alterations of CPP and its subsequent effects. The gastrointestinal mucosal barrier plays a pivotal role in the body's protection against luminal pathogens and antigenic molecules. The impairment of the gastrointestinal barrier function with massive bacterial translocation (BT) occurs during sepsis, both in human and in animal models. [1][2][3][4][5] In these circumstances, bacteria and their lysis products, such as lipopolysaccharide (LPS), gain access to portal and systemic circulations, producing critical deleterious effects. Sepsis is the most common cause of death for hospitalized patients. The gastrointestinal barrier includes secreted mucus and the epithelial cell layer itself, which prevent BT of intestinal flora through both transcellular and paracellular pathways.7 Tight junction (TJ) opening is the major limiting factor of the paracellular pathway. Examination of isolated human and rodent small intestine cells and cell lines have shown that TJ opening is driven by myosin light chain (MLC) phosphorylation, which depends on myosin light chain kinase (MLCK) activation. 8,9 MLC phosphorylation occurs within the perijunctional actomyosin ring and co-localizes with the TJ.9 Studies using an inducible active MLCK have shown that this activity is sufficient to activate the downstream events necessary for TJ regulation. 10Moreover MLCK-mediated regulation of TJ opening appears to be a common intermediate in a variety of physiological and pathophysiological pathways related to altered paracellular permeability both in vitro and in vivo. 10 -12 For example, enteropathogenic Escherichia coli infection causes diarrhea in children. An in vitro model has demonstrated that enteropathogenic E. coli dramatically ...

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Increased Intestinal Marker Absorption Due to Regional Permeability Changes and Decreased Intestinal Transit during Sepsis in the Rat

Abstract: The results suggest that the increased intestinal absorption during sepsis was due to regional permeability changes and prolonged intestinal transit.

Cited by 25 publications

References 29 publications

Overexpression of Fas and FasL Is Associated with Infectious Complications and Severity of Experimental Severe Acute Pancreatitis by Promoting Apoptosis of Lymphocytes

Overexpression of Fas and FasL Is Associated with Infectious Complications and Severity of Experimental Severe Acute Pancreatitis by Promoting Apoptosis of Lymphocytes

Sex steroid deficiency–associated bone loss is microbiota dependent and prevented by probiotics

Myosin Light Chain Kinase Is Involved in Lipopolysaccharide-Induced Disruption of Colonic Epithelial Barrier and Bacterial Translocation in Rats

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