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Results for “Intestinal Barrier Function”

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At least 1,099 records · Page 61Linked to original sources
PubMed2000

Gut permeability in patients with acute pancreatitis.

BACKGROUND: The bacterial contamination of pancreatic necrosis in acute pancreatitis is supposed to occur through translocation of intestinal bacteria. Increased gut permeability may be the initial phenomenon in this process. To test the hypothesis that gut permeability is increased in acute pancreatitis a clinical study was made where gut absorption and permeability were assessed with multi-sugar probes in patients with acute pancreatitis within 2 days after admission to hospital and again after recovery of disease. METHODS AND RESULTS: Twenty-three patients with acute pancreatitis and 20 healthy controls were studied. According to Atlanta classification, 15 patients had mild and 8 patients severe pancreatitis. Gut absorption, assessed as the 5-h urine excretion of L-rhamnose, D-xylose and 3-O-methylglucose, was decreased in patients with acute pancreatitis and more pronounced in patients with severe pancreatitis (L-rhamnose and D-xylose: P < 0.001; 3-O-methylglucose: P < 0.05). Gut permeability, assessed as the ratio of lactulose/L-rhamnose, was increased in severe pancreatitis (0.16 +/- 0.13, 0.07 +/- 0.03, 0.04 +/- 0.04; severe pancreatitis, mild pancreatitis, controls, respectively; P < 0.001 between three groups, P < 0.05 between pancreatitis groups). CONCLUSIONS: Gut absorption capacity is decreased and gut permeability is increased in patients with acute pancreatitis. Patients with severe pancreatitis may be more exposed to impaired gut barrier function.

Acute Disease↗
PubMed2006

Isolation, culture, and characterization of intestinal mast cells.

Mast cells are bone-marrow-derived tissue cells typically located at barrier sites of the body, such as skin, mucosal barriers, or blood barriers, that is, around blood vessels. This location suggests that mast cells might have a function as immunological "gate-keepers" or "watch dogs" and, indeed, some recent functional data support this idea. Mast cells derive from myeloid progenitors, but in contrast to other myeloid cells, they leave the bone marrow in an immature state; therefore, mast cells are not found in the blood under normal conditions. For full maturation, the tissue environment is necessary. Thus, mature mast cells can be only isolated from tissue such as skin or mucosal sites, which makes mast cell isolation rather complicated. Alternatively, mast cell progenitors can be isolated from the bone marrow, peripheral blood, or cord blood, which is easier but requires subsequent in vitro maturation of mast cells as far as possible using cytokines. This chapter describes a rather new technique of mast cell isolation from human intestinal mucosal tissue yielding approx 1-5 million pure and viable human mast cells suitable to perform functional and cell culture experiments.

Animals↗
PubMed1994

[Study on preserving intestinal function and the possible mechanism of hypermetabolic response following severe burn injury].

In order to approach the mechanism of hypermetabolic response following severe burn injury, a new animal model was developed with a specially bred miniswine (Guizhou species). Multiple catheterizations were applied for sampling different blood from portal, inferior mesenteric as will as jugular (central) veins. The animals were sustained with 30% III burn of TB-SA and divided randomly into early feeding group, given a complete diet beginning from 2 hours postburn (N = 6), and delayed feeding group, given the same diet initiating on 4 day postburn (N = 6). The results showed that compared with delayed feeding, early enteral feeding could strengthen the barrier function, decline the rate of translocation of bacteria and endotoxin from the gut to portal vein, reduce obviously blood TNF, CRP and catabolic-hormones, and significantly decrease REE (resting energy expenditure) and urinary 3-Mehis excretion. During the hypermetabolism (PBD7-10), the metabolic response mediated by "intestinal way" was at least 35%. The way of "intestinal tract--macrophages in liver--Hypermetabolism" is a possible mechanism of hypermetabolic response following severe burn injury, and the bacteria and endotoxin translocated from the gut, the active products (IL-1, TNF, etc) released by Kupffer's cells might be the mediating factors of the mechanism.

Animals↗
PubMed1996

Effect of early nutritional deprivation and diet on translocation of bacteria from the gastrointestinal tract in the newborn rat.

The gastrointestinal (GI) barrier function is immature in the preterm neonate and might thus facilitate translocation of enteric bacteria and gut-derived septicemia. Circumstantial evidence suggests that bacterial uptake from the intestine may be further enhanced by an alteration of the host nutritional status. To test this hypothesis, neonatal rats were fed normal or restricted amounts of either breast milk or of a rat milk-simulated formula for 3-5 d. At the end of the study, various sections of the GI tract, mesenteric lymph nodes, liver, spleen, and blood were analyzed for bacteria using standard microbiologic procedures. Normal breast feeding was associated with bacterial translocation to mesenteric lymph nodes and in some cases to liver or spleen in 27% of rats, whereas all bacterial cultures were negative in a control group killed immediately after birth. Restricted breast feeding did not increase translocation compared with normal breast feeding. By contrast, feeding normal or restricted amounts of formula increased the numbers of gut bacteria by 2-3 logs, altered the morphology of the small intestinal mucosa, and resulted in ample bacterial translocation to the mesenteric lymph nodes and to systemic organs including the blood. Bacterial translocation may normally occur in suckling neonatal rats and is not increased by food restriction. Artificial feeding dramatically enhances translocation of gut bacteria.

Animals↗
PubMed2005

[Helicobacter pylori infection in patients with chronic hives and asthma].

Difficulties in treatment of allergic diseases (ADs) are often determined by the fact that the origin of the illness is impossible to establish. Foreign researchers have demonstrated a correlation between Helicobacter pylori (HP) persistence and such conditions as chronic relapsing urticaria (CRLU), Quincke's edema (QO) and respiratory manifestations of allergy (usually bronchial asthma (BA)). HP may participate in the forming of ADs in three possible ways: 1) the bacteria interact with mast cells, and thus are able to initiate mediator liberation; 2) being full antigens, the bacteria themselves are able to cause allergy; 3) the infection process development impairs the barrier function of the alimentary tract mucosa, thus impairing food processing. This creates conditions for allergic food particles to enter bloodstream, which is facilitated by inflammatory lesions of the intestinal tract, protozoal and helminthic invasion, and dysbacteriosis. The aim of the study was to determine how frequently patients with CRU, QO and BA have HP invasion and develop intestinal microflora disbalance, as well as to find out whether there is a correlation between HP infection and alterations in the IgE-system, and establish anti-HP therapy effects, measuring the levels of anti-helicobacter antibody and IgE before and after the treatment. The study revealed HP invasion in 89.2% of patients with chronic ADs; 96.7% of the subjects had disturbances of microbiocenosis; total IgE level correlated with the allergic process activity and anti-helicobacter antibody level; eradicational therapy was more effective when included proton pump inhibitor, clarithromycin and flemoxin than when de-nol, clarithromycin and flemoxin were administered. According to the results of the study, anti-helicobacter therapy allows more effective treatment of patients with relapsing ADs and HP infection.

Adolescent↗
PubMed1989

[The reaction of the endocrine cells of the gastrointestinal tract in response to exposure to 3,6-dichloropicolinic acid].

Silver-impregnated argentaffin cells both Ec, D1, G, P, S and K enteroendocrine cell types of rat gastrointestinal mucosa were investigated under light and electron microscopy after single oral administration of 3,6-dichloropicolinic acid. As a result, in pyloric-duodenal region Ec cells after a period of 1 hour had intensively secreted hormones. Ultrastructurally their cytoplasm and secretory granules were covered by expressed vacuolization. These data hypothetically elucidate the role of the endocrine regulations in developing barrier function of the gastrointestinal epithelium.

Animals↗
PubMed1996

[Hydrolases of the digestive and nondigestive organs in rhesus macaque monkeys].

Distribution of activity of a wide range of hydrolases was characterised in the duodenum, ileum, jejunum, and colon, as well as in the liver, kidney and spleen in Macaca rhesus. The findings suggest presence of a complex enzyme system performing the membrane and intracellular hydrolysis of nutritional substances, in the small intestine of the primates as well as other mammals. This system, along with the hydrolases of the colon and non-digestive organs, seems to function as an enzymatic barrier.

Animals↗
PubMed2006

Immunogenetic phenotypes in inflammatory bowel disease.

The currently accepted etiopathogenic hypothesis suggests that the chronic intestinal inflammation and related systemic manifestations characteristic of inflammatory bowel disease (IBD) are due to an overly aggressive or pathologic immune response to resident luminal bacterial constituents. Predisposing factors are genetic dysregulation of mucosal immune responses and/or barrier function, with onset triggered by environmental stimuli. These factors and their interactions may also be important determinants of disease phenotype and disease progression. The emergence of immunogenetic phenotypes lends support to the proposed hypothesis that susceptibility genes regulate distinct immune processes, driven by luminal antigens, expressed as specific immune phenotypes which in turn influence clinical phenotypes in IBD patient.

Antibodies, Bacterial↗
PubMed2004

Do surface-active lipids in food increase the intestinal permeability to toxic substances and allergenic agents?

The incidence of many common diseases has increased during the last decades. High fat intake is a risk factor for many diseases. We propose that some of the negative effects of fat are caused by lipid-induced damage of the gastrointestinal epithelium, thus compromising the epithelial function as a barrier for passage of toxic substances and allergenic agents to the circulatory system. Monoglycerides (MGs), phospholipids and fatty acids (FAs) are surface-active molecules that in pharmaceutical studies act as permeability enhancers for hydrophilic drugs with low absorption. Three possible mechanisms were proposed: (a) lipid-induced alterations in intracellular events may cause destabilization of tight junctions between the GI epithelial cells, (b) lipids may destabilize cell membranes, (c) lipids cause intestinal cell damage, which increase the permeability of the GI epithelium. These "side effects" of lipids may partly explain the association between fat intake and disease observed in epidemiological studies.

Administration, Oral↗
PubMed1996

Intestinal permeability in the ileal pouch.

BACKGROUND: Villous atrophy, mucin changes ('colonic metaplasia'), and chronic inflammation occur to varying degrees in all patients with ileal pouchanal anastomosis whereas acute inflammation (pouchitis) affects a subgroup of patients with prior ulcerative colitis. AIM: To measure epithelial barrier function looking for possible functional adaptation in ileal 'pouch' mucosa. PATIENTS: Patients with an ileal pouch prior to ileostomy closure (n = 12), functioning pouch (n = 14), pouchitis (n = 8), and ulcerative colitis (n = 12) were assessed. METHODS: 51Cr-EDTA was administered into the 'pouch' or rectum and urinary recovery over 24 hours was taken as an indication of permeability (barrier function). Histological analysis of 'pouch' biopsy specimens was undertaken. RESULTS: Mucosal permeability is decreased from median 9.4% (range 5.4% to 39.1%) to 1.4% (range 0.38% to 2.2%) after ileostomy closure (p < 0.002) with levels being negatively correlated with two histological parameters of colonic metaplasia-mucin changes (p = 0.03) and villous atrophy (p = 0.05). Pouchitis was associated with increased permeability 5.9% (1.9% to 19.5%) compared with healthy 'pouch' 1.4% (0.35 to 2.2%) (p < 0.006). CONCLUSION: Despite the presence of chronic inflammation in the mature 'pouch' functional adaptation with reduced permeability occurs in conjunction with colonic metaplasia.

Biopsy↗
PubMed2000

Role of breast cancer resistance protein in the bioavailability and fetal penetration of topotecan.

BACKGROUND AND METHODS: Breast cancer resistance protein (BCRP/MXR/ABCP) is a multidrug-resistance protein that is a member of the adenosine triphosphate-binding cassette family of drug transporters. BCRP can render tumor cells resistant to the anticancer drugs topotecan, mitoxantrone, doxorubicin, and daunorubicin. To investigate the physiologic role of BCRP, we used polarized mammalian cell lines to determine the direction of BCRP drug transport. We also used the BCRP inhibitor GF120918 to assess the role of BCRP in protecting mice against xenobiotic drugs. Bcrp1, the murine homologue of BCRP, was expressed in the polarized mammalian cell lines LLC-PK1 and MDCK-II, and the direction of Bcrp1-mediated transport of topotecan and mitoxantrone was determined. To avoid the confounding drug transport provided by P-glycoprotein (P-gp), the roles of Bcrp1 in the bioavailability of topotecan and the effect of GF120918 were studied in both wild-type and P-gp-deficient mice and their fetuses. RESULTS: Bcrp1 mediated apically directed transport of drugs in polarized cell lines. When both topotecan and GF120918 were administered orally, the bioavailability (i.e., the extent to which a drug becomes available to a target tissue after administration) of topotecan in plasma was dramatically increased in P-gp-deficient mice (greater than sixfold) and wild-type mice (greater than ninefold), compared with the control (i.e., vehicle-treated) mice. Furthermore, treatment with GF120918 decreased plasma clearance and hepatobiliary excretion of topotecan and increased (re-)uptake by the small intestine. In pregnant GF120918-treated, P-gp-deficient mice, relative fetal penetration of topotecan was twofold higher than that in pregnant vehicle-treated mice, suggesting a function for BCRP in the maternal-fetal barrier of the placenta. CONCLUSIONS: Bcrp1 mediates apically directed drug transport, appears to reduce drug bioavailability, and protects fetuses against drugs. We propose that strategic application of BCRP inhibitors may thus lead to more effective oral chemotherapy with topotecan or other BCRP substrate drugs.

ATP Binding Cassette Transporter, Subfamily G, Mem↗
PubMed2006

Probiotics and inflammatory bowel diseases.

Enteric microflora profiles vary considerably between active inflammatory bowel diseases (IBD) and healthy conditions. Intestinal microflora may partake in the pathogenesis of IBD by one or some ways: specific pathogenic infection induces abnormal intestinal mucosal inflammation; aberrant microflora components trigger the onset of IBD; abnormal host immune response loses normal immune tolerance to luminal components; luminal antigens permeate through the defective mucosal barrier into mucosal lamina propria and induce abnormal inflammatory response. Preliminary studies suggest that administration of probiotics may be benefit for experimental colitis and clinical trials for IBD. Researches have been studying the function of probiotics. Introduction of probiotics can balance the aberrant enteric microflora in IBD patients, and reinforce the various lines of intestinal defence by inhibiting microbial pathogens growth, increasing intestinal epithelial tight junction and permeability, modulating immune response of intestinal epithelia and mucosal immune cells, secreting antimicrobial products, decomposing luminal pathogenic antigens.

Bacteria↗
PubMed2006

Hypoxia/reoxygenation impairs glucose absorption and cAMP-mediated secretion more profoundly than glutamine absorption and Ca2+/PKC-mediated secretion in rat ileum in vitro.

BACKGROUND: Intestinal ischemia and reperfusion may lead to profuse secretion of water and electrolytes. The underlying mechanisms have been related to increased hydrostatic pressure, to denudation of intestinal villi, and, recently, to adenosine-mediated enhancement of chloride secretion. METHODS: We studied the effects of hypoxia and reoxygenation on baseline electrophysiologic parameters; on glucose- and glutamine-induced absorption; on secretion induced by carbachol, histamine, and forskolin; and on epithelial barrier function to disodium-fluorescein and horseradish peroxidase in rat ileum mounted in Ussing chambers. RESULTS: We observed that 30 minutes of hypoxia followed by 60 minutes of reoxygenation differentially affected glucose and glutamine absorption to 11% and 42%, respectively, of control values. Cyclic adenosine monophosphate-mediated secretion induced by forskolin was reduced to 9% of controls. In contrast, Ca(2+)/protein kinase C-mediated secretion induced by carbachol or histamine was reduced only to 35% to 48% of controls. Furthermore, the epithelium fully was capable of maintaining its barrier function to small and large permeability probes, even after 90 minutes of hypoxia. CONCLUSIONS: We conclude that hypoxia and reoxygenation differentially impair nutrient absorption, corroborating recent absorption data in in vivo models of ischemia, and that it differentially affects secretory capacity in crypts, dependent on the intracellular messenger pathway. The relative persistence of Ca(2+)/protein kinase C-mediated secretion to hypoxia and reoxygenation indicates that secretagogues that activate this pathway play a significant role in the intraluminal fluid sequestration and diarrhea observed after intestinal ischemia and reperfusion.

Absorption↗
PubMed1997

Gut dysfunction in critically ill patients: a review of the literature.

BACKGROUND: Critically ill patients are susceptible to injury of the intestinal mucosa, changes in gut permeability, and failure of intestinal defense mechanisms. These conditions put the patients at risk for infection and multiple organ dysfunction syndrome. Specific therapies are needed to prevent gut failure during critical illness. OBJECTIVE: The purpose of this literature review is to provide a better understanding of the normal defense mechanisms of the gut and alterations associated with ischemia-reperfusion injury, risk of infection, and the link to multiple organ dysfunction syndrome in critically ill patients. Implications for early enteral stimulation and nutrition are included. METHODS: Medical and nursing studies on the intestinal response to critical illness and on the implications for early enteral nutrition in critically ill patients were reviewed. RESULTS: Significant advances have been made in understanding the normal defense mechanisms of the gut, including barrier and immune functions. Translocation of bacteria, mediators of the inflammatory response, and the microcirculation play a role in the response to critical illness. Enteral nutrition that includes glutamine and arginine enhances gut function and improves patients' outcomes in some clinical states. DISCUSSION: Further research should focus on specific strategies to enhance gut function, prevent loss of gut integrity, and improve patients' outcomes. These strategies include maintaining mesenteric blood flow, using gastric tonometry to assess oxygenation, inhibiting inflammatory mediators, and using growth factors to modify the metabolic state in patients who are critically ill.

Bacterial Translocation↗
PubMed2002

Ecto-5'-nucleotidase (CD73) regulation by hypoxia-inducible factor-1 mediates permeability changes in intestinal epithelia.

Under conditions of limited oxygen availability (hypoxia), multiple cell types release adenine nucleotides in the form of ATP, ADP, and AMP. Extracellular AMP is metabolized to adenosine by surface-expressed ecto-5'-nucleotidase (CD73) and subsequently activates surface adenosine receptors regulating endothelial and epithelial barrier function. Therefore, we hypothesized that hypoxia transcriptionally regulates CD73 expression. Microarray RNA analysis revealed an increase in CD73 and ecto-apyrase CD39 in hypoxic epithelial cells. Metabolic studies of CD39/CD73 function in intact epithelia revealed that hypoxia enhances CD39/CD73 function as much as 6 +/- 0.5-fold over normoxia. Examination of the CD73 gene promoter identified at least one binding site for hypoxia-inducible factor-1 (HIF-1) and inhibition of HIF-1alpha expression by antisense oligonucleotides resulted in significant inhibition of hypoxia-inducible CD73 expression. Studies using luciferase reporter constructs revealed a significant increase in activity in cells subjected to hypoxia, which was lost in truncated constructs lacking the HIF-1 site. Mutagenesis of the HIF-1alpha binding site resulted in a nearly complete loss of hypoxia-inducibility. In vivo studies in a murine hypoxia model revealed that hypoxia-induced CD73 may serve to protect the epithelial barrier, since the CD73 inhibitor alpha,beta-methylene ADP promotes increased intestinal permeability. These results identify an HIF-1-dependent regulatory pathway for CD73 and indicate the likelihood that CD39/CD73 protects the epithelial barrier during hypoxia.

5'-Nucleotidase↗
PubMed2004

Antagonistic activities of lactobacilli and bifidobacteria against microbial pathogens.

The gastrointestinal tract is a complex ecosystem that associates a resident microbiota and cells of various phenotypes lining the epithelial wall expressing complex metabolic activities. The resident microbiota in the digestive tract is a heterogeneous microbial ecosystem containing up to 1 x 10(14) colony-forming units (CFUs) of bacteria. The intestinal microbiota plays an important role in normal gut function and maintaining host health. The host is protected from attack by potentially harmful microbial microorganisms by the physical and chemical barriers created by the gastrointestinal epithelium. The cells lining the gastrointestinal epithelium and the resident microbiota are two partners that properly and/or synergistically function to promote an efficient host system of defence. The gastrointestinal cells that make up the epithelium, provide a physical barrier that protects the host against the unwanted intrusion of microorganisms into the gastrointestinal microbiota, and against the penetration of harmful microorganisms which usurp the cellular molecules and signalling pathways of the host to become pathogenic. One of the basic physiological functions of the resident microbiota is that it functions as a microbial barrier against microbial pathogens. The mechanisms by which the species of the microbiota exert this barrier effect remain largely to be determined. There is increasing evidence that lactobacilli and bifidobacteria, which inhabit the gastrointestinal microbiota, develop antimicrobial activities that participate in the host's gastrointestinal system of defence. The objective of this review is to analyze the in vitro and in vivo experimental and clinical studies in which the antimicrobial activities of selected lactobacilli and bifidobacteria strains have been documented.

Animals↗
PubMed1992

Role of alcohol abuse in nutritional immunosuppression.

Nutritional status is an important determinant of the host resistance against infections and tumors. Alcohol interferes in various ways with the complex system of nutritional immunomodulation. Alcohol acts directly on mechanical barriers in the gastrointestinal tract and increases permeability of intestinal walls, which results in a reduced exclusion of immunogenic material in the intestine. Alcohol further affects granulocytopoiesis and suppresses various immune functions. Indirect effects on the immune response are caused by alcohol-induced malnutrition. Heavy alcohol abuse is associated with a high energy intake derived by alcohol and an inadequate intake of protein, vitamins and minerals. In addition, alcohol abuse impairs absorption, utilization, storage and excretion of nutrients, which together with inadequate nutrient intakes results in nutritional immunosuppression. The high incidence of infections in alcoholics could be one consequence of the alcohol-induced immunosuppression.

Alcoholism↗