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Results for “Intestinal barrier”

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At least 127 records · Page 7Linked to original sources
PubMed1996

[The dietary correction of the permeability of the protective intestinal barrier in rats after gamma irradiation].

400 to 700 rad irradiation with gamma-rays significantly increased the intestinal permeability for ovalbumin and polyethylene glycol in rats. Consumption of cow's milk with a protein concentrate for 14 days prior to irradiation helped to normalise the disturbed permeability. The findings suggest the possibility of prophylactic use of milk for risk group subjects with acute or chronic radiation injuries.

Animals↗
PubMed1997

Gastro-intestinal toxicity related to bone marrow transplantation: disruption of the intestinal barrier precedes clinical findings.

The intensive cytotoxic treatment given in connection with bone marrow transplantations induces severe injury to the gut consistent with an increase in intestinal permeability. Currently, extent of the gut injury is assessed by inspecting the mouth and recording symptoms deriving from the gastro-intestinal tract. The aims of this study were to evaluate whether changes in permeability correlate with clinical assessment of gut toxicity, according to the WHO criteria, and also to examine the duration of intestinal permeability after high-dose chemotherapy. In 18 consecutive patients undergoing bone marrow transplantation, gastrointestinal permeability was assessed by a 51Cr-EDTA absorption test before the start of cytotoxic treatment, and 4, 7, 10 and 14 days after stem-cell infusion. In another seven patients, permeability was assessed 2 days after the start of cytotoxic treatment, and 1, 7 and 14 days after stem cell infusion. During the same period, oral- and non-oral clinical toxicity according to the WHO criteria were recorded. Permeability increased significantly 2 days after the start of cytotoxic treatment (P < 0.05), on day 1 (P < 0.05), on day 4 (P < 0.0005), on day 7 (P < 0.0005) and on day 10 (P < 0.005) after stem cell infusion, compared with pre-treatment permeability. Despite significant barrier dysfunction, clinical toxicity was very moderate in the early transplantation course. Gastro-intestinal, but not oral clinical toxicity requiring therapy, was consistent with a significant increase in permeability compared with no clinical toxicity or toxicity not requiring therapy. Similarly, cumulative gastro-intestinal, but not oral toxicity correlated positively with the increase in permeability. The permeability test was unable to predict the severity of the clinical gastro-intestinal toxicity.

Adult↗
PubMed2000

Role of M cells in intestinal barrier function.

M cells are known as specialized epithelial cells of the follicle-associated epithelium of the gastrointestinal tract. As M cells have a high capacity for transcytosis of a wide range of microorganisms and macromolecules, they are believed to act as an antigen sampling system. The primary physiological role of M cells seems to be the rapid uptake and presentation of particular antigens and microorganisms to the immune cells of the lymphoid follicle to induce an effective immune response. In contrast to absorptive enterocytes, M cells do not exert direct defense mechanisms to antigens and pathogens in the gut lumen. Therefore, they provide functional openings of the epithelial barrier. Although M cells represent a weak point of the epithelial barrier, even under noninflamed conditions, there seems to be a balance between antigen uptake and immunological response. The low number of M cells in the gastrointestinal tract and the direct contact to immune cells in the lamina propria usually prevent the occurrence of mucosal inflammation. During chronic intestinal inflammation we observe an increase of M cell number and apoptosis selectively in M cells. M cell damage seems to be responsible for the increase of the uptake of microorganisms that is observed during intestinal inflammation. Under inflammatory conditions in the intestine, the maintenance of the epithelial barrier is broken and M cells seem to play a major role during this process.

Animals↗
PubMed2007

Commensal bacteria do translocate across the intestinal barrier in surgical patients.

BACKGROUND: The "gut origin of sepsis" hypothesis proposes that enteric bacteria may cause sepsis at distant extra-intestinal sites. Whilst there is much circumstantial evidence to support this hypothesis, there is no conclusive proof in humans. The nature of translocating bacteria remains unclear. The aim of this study was to establish the origin of Escherichia coli (E. coli) cultured from mesenteric lymph nodes (MLN) and determine if they belonged to any recognized pathotypes known to cause infections in humans. METHODS: MLN and faecal samples were obtained from 98 patients undergoing colonic resection. E. coli were isolated from 9/98 MLN samples. DNA fingerprints of MLN isolates were compared with faecal isolates from the same patient. MLN isolates were tested for adherence and invasion using HEp-2 epithelial cells, and screened for DNA markers indicative of different pathotypes of E. coli. MLN isolates were also tested for internalisation into Caco-2 cells. RESULTS: All the nine E. coli cultured from MLNs were found to have identical DNA fingerprints to at least one and often several E. coli isolates cultured from faecal samples of the same patient. 8/9 (89%) MLN isolates were weakly adherent and 2/9 (22.2%) were invasive. 8/9 (89%) tested negative for DNA markers. All the nine MLN strains were internalised by Caco-2 cells. CONCLUSION: This study confirms the gut origin of translocating bacteria. Most translocating E. coli do not belong to any recognised pathotype and are therefore normal commensal microflora. Our results suggest that bacterial translocation is more dependent upon the gut epithelium rather than the virulence properties of resident enteric bacteria.

Adult↗
PubMed2006

Impairment of the intestinal barrier by ethanol involves enteric microflora and mast cell activation in rodents.

Alcohol hepatic toxicity in heavy drinkers is associated with high endotoxin blood levels and increased intestinal permeability. Because endotoxins can cross damaged mucosa, we investigated the mechanisms through which ethanol impairs the colonic epithelium of rats submitted to acute alcohol intake. Colonic permeability to (51)Cr-ethylenediamintetraacetic acid was increased 24 hours after 3.0 g/kg ethanol intake (3.2 +/- 0.2% versus 2.2 +/- 0.2%) and was associated with significant endotoxemia. Antibiotics and doxantrazole (a mast cell membrane stabilizer) significantly inhibited the effect of ethanol. Two hours after intake, plasma concentrations of ethanol were twofold higher in antibiotic-treated rats than in controls (155.8 +/- 9.3 mg/dl versus 75.7 +/- 7.6 mg/dl, P < 0.001). Lumenal concentrations of acetaldehyde were markedly increased after ethanol intake (132.6 +/- 31.6 micromol/L versus 20.8 +/- 1.4 micromol/L, P < 0.05) and antibiotics diminished this increase (86.2 +/- 10.9 micromol/L). In colonic samples mounted in Ussing chambers, acetaldehyde but not ethanol increased dextran flux across the mucosa by 54%. Doxantrazole inhibited the effect of acetaldehyde. This study demonstrates that an acute and moderate ethanol intake alters the epithelial barrier through ethanol oxidation into acetaldehyde by the colonic microflora and downstream mast cell activation. Such alterations that remain for longer periods could result in excessive endotoxin passage, which could explain the subsequent endotoxemia frequently observed in patients with alcoholic liver disease.

Acetaldehyde↗
PubMed1998

In vitro and in vivo evaluations of intestinal barriers for the zwitterion L-767,679 and its carboxyl ester prodrug L-775,318. Roles of efflux and metabolism.

The barriers to oral delivery of the hydrophilic zwitterion L-767, 679 (I) and its carboxyl ester prodrug L-775,318 (II) were examined. In the Caco-2 cell model, transport of II, but not I, was strongly oriented in the secretory direction. The basal-to-apical transport of II displayed saturable kinetics and was markedly inhibited by verapamil and quinidine, known P-glycoprotein inhibitors. In Caco-2 cells, metabolism of I was not observed, whereas hydrolysis of II was modest (</=20%). In the in situ rat intestinal loop model, verapamil did not affect the absorption of I but significantly increased the absorption of II. I was resistant to intestinal metabolism, whereas II underwent hydrolysis partially in rat lumen but more extensively in rat intestinal tissue and blood. In vitro metabolism studies indicated that verapamil also inhibited the hydrolysis of II in rats. The inhibition was relatively specific for the intestinal and not the luminal esterases. These results suggested that the intestinal absorption of I was limited not by intestinal efflux or metabolism but more likely by the low lipophilicity of I. However, an efflux system, likely mediated by P-glycoprotein, played an important role in limiting the absorption of II. In rats, metabolism served as an additional barrier to the absorption of II. Verapamil increased the intestinal absorption of the prodrug by inhibiting the efflux system in the two models studied, as well as possibly inhibiting metabolism in rats. For the first time, secretory transport was identified as a cause of the failure to increase the absorption of a lipophilic and cationic prodrug developed to overcome the absorption problem.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1999

[Permeability of intestinal barrier fo macromolecules in patients with Crohn's disease and ulcerative colitis].

Ovalbumin loading enzyme immunoassay was made in 44 patients with ulcerative colitis (UC) and 8 patients with Crohn's disease (CD). Enhanced intestinal permeability for macromolecules was found in 87.5 and 65.9% of patients with CD and UC, respectively. Blood serum of UC patients suffering from combination of food intolerance with dysbacteriosis contained ovalbumin in amounts exceeding those in patients without the above disorders 3.4 times (p < 0.05). No significant relationship existed between UC patients' high intestinal permeability and such indices as age, duration of the disease, intestinal lesion extension, administration of corticosteroids. It was found desirable to include ovalbumin intestinal permeability test in examination of UC and CD patients to differentiate treatment policy.

Adolescent↗