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Results for “Intestinal Barrier Function”

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PubMed2006

Coordinated epithelial NHE3 inhibition and barrier dysfunction are required for TNF-mediated diarrhea in vivo.

Acute T cell-mediated diarrhea is associated with increased mucosal expression of proinflammatory cytokines, including the TNF superfamily members TNF and LIGHT. While we have previously shown that epithelial barrier dysfunction induced by myosin light chain kinase (MLCK) is required for the development of diarrhea, MLCK inhibition does not completely restore water absorption. In contrast, although TNF-neutralizing antibodies completely restore water absorption after systemic T cell activation, barrier function is only partially corrected. This suggests that, while barrier dysfunction is critical, other processes must be involved in T cell-mediated diarrhea. To define these processes in vivo, we asked whether individual cytokines might regulate different events in T cell-mediated diarrhea. Both TNF and LIGHT caused MLCK-dependent barrier dysfunction. However, while TNF caused diarrhea, LIGHT enhanced intestinal water absorption. Moreover, TNF, but not LIGHT, inhibited Na+ absorption due to TNF-induced internalization of the brush border Na+/H+ exchanger NHE3. LIGHT did not cause NHE3 internalization. PKCalpha activation by TNF was responsible for NHE3 internalization, and pharmacological or genetic PKCalpha inhibition prevented NHE3 internalization, Na+ malabsorption, and diarrhea despite continued barrier dysfunction. These data demonstrate the necessity of coordinated Na+ malabsorption and barrier dysfunction in TNF-induced diarrhea and provide insight into mechanisms of intestinal water transport.

Animals↗

PubMed2001

[Metabolic disorders in nonspecific inflammatory bowel diseases].

The primary function of the gastrointestinal system is to assist the intake and further processing of food and liquids. Besides that, it forms an anatomical barrier between the external environment and internal milieu. It is also highly important for its paracrine and endocrine function. Inflammatory bowel diseases, which frequently cause a gastrointestinal failure, form a specific group. Most frequently it is the ulcerative colitis and Crohn's disease. Impaired integrity of the gastrointestinal mucosa and failure of protective mechanisms lead to the increased permeability of the intestinal wall for antigens derived from food, saprophytic bacteria and pathogenic microorganisms. When the gastrointestinal failure is threatening, factors determining its residual function become more important. As decisive reveals the severity and location of the primary disease. Previous surgeries and adaptation of the residual part of the gastrointestinal system are important, as well as the possibility of peroral or enteral nutrient intake. Depending on the presence of risk factors and the degree of residual gut function, some complications can be expected: dehydration, mineral disorders, symptoms of protein and energy depletion, infection, and multiple organ dysfunction syndrome. It is highly important to decide whether the gastrointestinal system will be included into or excluded from the process of realimentation. Critically ill patients with inflammatory bowel diseases should be treated at an intensive care unit.

Deficiency Diseases↗

PubMed1992

Cytochemical and immunocytochemical characterization of a fibrillar network (GP2) in pancreatic juice: possible role as a sieve in the pancreatic ductal system.

The secretory product of the exocrine pancreas contains sedimentable and non-sedimentable materials. Electron microscopy of the pellet obtained after ultracentrifugation reveals two major components: microvesicles (pancreasomes) and a fibrillar network of small mesh size. Negative staining of an unfixed pellet demonstrated that these structures are not fixation artifacts. Cytochemical analysis showed that pancreasomes are reactive to osmication and uranyl acetate staining, whereas the fibrillar network was unreactive thereby indicating that the latter does not contain lipids; however, lead citrate staining reveals the network. Alcian blue, known to bind sulfate groups of mucosubstances, reacted strongly with the fibrillar network. The pellet was also characterized by immunocytochemistry with specific antibodies to amylase and glycoprotein 2 (GP2). Both antibodies were located only on the fibrillar network. Washing of the pellet with 100 mM KCl-250 mM NaBr had little effect on GP2 content, but reduced considerably alpha-amylase associated with the reticular matrix. It appeared that GP2 was the major component of the scaffolding that gives rise to the fibrillar network and that other proteins such as alpha-amylase could reversibly bind to it. When double-labeling immunocytochemistry was carried out on the unwashed pellet, labeling of the first antigen reduced the labeling of the second. Removal of amylase by washing the pellet increased the GP2 signal. These results indicate that amylase is bound on the GP2 network. Although the function of the GP2 network is still not clearly defined several possibilities could be envisaged at the level of the pancreatic duct system: 1) The network could drain off any aggregates or precipitates forming in small ducts. 2) The small mesh of the network would present a physical barrier to infecting bacteria that could enter into the duct system from the intestine, especially in conditions of low flow rates. 3) The network may exert a mechanical pressure on the membranes bordering the acinar lumen and small ducts thereby preventing their collapse in basal conditions.

Animals↗

PubMed1989

[Microbial ecology of the intestines in health and in pathology].

Bifidoflora constitute 85--95 per cent of the large intestine microbiocenosis in children under 1 year of age. Bacteroides are not specific of children under 6 months of age. Lactobacilli, lactic acid streptococci, colon bacilli, enterococci and staphylococci (saprophytic, epidermal) constitute not more than 15 per cent. The predominating group peculiar of eubiosis in adults includes bifidobacteria and bacteroides. Changes in human autoflora are often induced by such factors as impaired ecology, stress, uncontrolled use of antibacterial drugs, radio- and chemotherapy, etc. Dysbacteriosis (first of all lower quantitative contents of bifidoflora) has an unfavourable effect on the intestine secretory function, absorption and certain indices of protein, lipid and mineral metabolism, vitamin synthesizing and fermentative functions and leads to disfunction of the gastrointestinal tract. It is a cause of persisting and relapsing infections in children and adults. High and optimal levels of bifidoflora in the intestine usually prevent the pathogenic action of pathogens. Lysozyme of digestive secretion and secretory immunity with immunoglobulin A prevalence also play an important role in the complicated mechanism of the protective barrier. The use of bacterial preparations such as bifidumbacterin, lactobacterin or bifilact for stabilization and recovery of high bifidoflora levels is indicated in all the cases with impaired microbiocenosis of the intestine.

Adult↗

PubMed1996

The effect of methotrexate on the expression of a cysteine protease inhibitor (type 2 cystatin) in rat sebaceous glands.

The purpose of this study was to assess whether rat cystatin S, a cysteine proteinase inhibitor, is present in rat sebaceous glands, and to measure the effects of methotrexate on the expression of cystatin in these glands. With methotrexate treatment, the number of skin sebaceous cells expressing cystatin increased from 13.9% to 34.3% (P < .05). A smaller increase (from 15.3% to 23.9%; P = .1) was observed in Zymbal sebaceous glands. Type 2 cystatin could not be detected in the major salivary glands, nor in trachea, lung, stomach, small intestine, large intestine, spleen, liver, kidney, or pancreas, in any of the rats given either saline or methotrexate. Our results suggest that type 2 cystatin is a constituent of normal sebaceous glands, and that the amount of cystatin present in these glands increases with methotrexate administration. We speculate that, in addition to the protective functions ascribed to sebaceous lipids, sebum may augment the physical barrier of skin through secretion of cysteine proteinases that may be pharmacologically modulated.

Animals↗

PubMed2002

Age-related association of small intestinal mucosal enteropathy with nutritional status in rural Gambian children.

Small bowel enteropathy (assessed by the lactulose (L) : mannitol (M) permeability test) is a major factor in infant growth faltering and malnutrition in The Gambia. However, little is known about its persistence and nutritional effect beyond 2 years of age. This was addressed by two cross-sectional studies of intestinal permeability and nutritional status in 162 residents, aged 2-60 years, living in three villages in rural Gambia. L:M ratio was found to be highest in the youngest children and although there was a significant improvement with age (P<0.0001), values were always greater than the range found in UK counterparts. M recovery (mean value 5.68 (se 0.12) %) was at all times between one-third and one-half of expected UK values and showed no improvement with age. Gut barrier function, assessed by L uptake, improved with age (P<0.001) and fell within the UK normal range beyond age 10 years. Both the L:M permeability ratio and L recovery were significantly associated with height-for-age z-scores and -0.22 respectively, P<0.001), a relationship that persisted throughout childhood and into adulthood. Change in height-for-age z-score between the two visits was also related to the L:M ratio P=0.018). The close within-subject correlation of permeability variabilities between the two visits suggests a long-term persistence of enteropathy within individuals. It appears that the small bowel enteropathy previously described in Gambian infants persists through to adulthood. Although the lesion improves with age, the relationship between attained height and L:M permeability raises the possibility that enteropathy may continue to limit growth throughout childhood and puberty.

Adolescent↗

PubMed1997

Ulcerative colitis: an epithelial disease?

There is now considerable evidence that abnormalities of the structure and function of the colonic epithelium are present in patients with ulcerative colitis and that many of these may occur independently of mucosal inflammation. It is proposed that epithelial abnormalities are the central defect that underlie the development of mucosal inflammation and its chronicity. A simple model for pathogenesis is proposed in which inflammation develops only when epithelial barrier function is impaired to an extent which permits the influx of luminal pro-inflammatory molecules to the lamina propria. Several candidate hypotheses regarding the molecular basis for the abnormality are addressed. The mechanism by which the barrier function is critically impaired involves the interaction of the abnormal epithelium with luminal, mucosal and systemic factors. Focusing on the epithelium would potentially lead to a conceptually different management approach and the development of novel therapeutic strategies.

Colitis, Ulcerative↗

PubMed1994

Bacterial translocation: the influence of dietary variables.

Transmucosal passage of bacteria in critically ill patients may lead to a significant incidence of systemic sepsis. This has attracted much clinical interest, as it has been shown that malnutrition in itself, impairs various aspects of barrier function. Bacterial translocation is increased in animal models where nutrients are given by the parenteral route, while enteral feeding reverses this. Translocation is also considerably increased in response to a non-lethal endotoxin challenge, if there is pre-existing protein energy malnutrition. Similar results have been obtained where the insult is caused by the inflammatory agent, zymosan. Dietary fibre reduces the deleterious effects of either agent on translocation, although the type of fibre is important. Bulk forming but non-fermentable fibres are more effective than easily fermentable types (for example, pectin). Glutamine was not effective in preventing elemental diet induced bacterial translocation. Thus, although fermentable fibre and glutamine have positive effects on mucosal mass, they do not affect translocation. Enteral nutrition thus seems to be superior to parenteral nutrition in maintaining the functional barrier of the gut. A clearer understanding of the physiology of these effects may lead to use of specifically modified enteral diets in the critically ill patient.

Animals↗

PubMed1987

The role of uvomorulin in the formation of epithelial occluding junctions.

We have used an assay for the recovery of transepithelial resistance to identify proteins involved in the formation of the epithelial occluding barrier. The occluding junctions of high resistance monolayers of strain I MDCK cells (greater than 2500 ohm X cm2) were opened briefly and reversibly by removal of Ca2+ from the bathing medium. We screened for monoclonal antibodies which could inhibit the recovery of resistance upon Ca2+ readdition. One such monoclonal antibody, rrl, was obtained which recognizes a uvomorulin-like (or L-CAM-like) polypeptide in MDCK cells. Uvomorulin may be primarily, if not entirely, responsible for the Ca2+ dependence of occluding junction integrity. The maintenance of transmonolayer resistance had the same divalent cation selectivity as the conformational change shown by the uvomorulin molecule. In contrast to its exclusive localization to the zonula adherens of small intestinal cells, we found uvomorulin to be distributed over much of the lateral plasma membrane of MDCK cells and dog hepatocytes. The role of extrajunctional uvomorulin in these cells is not understood. Treatment of intact, high resistance monolayers of MDCK cells with antibody rr1 failed to induce a loss of resistance even though the antibody had access to uvomorulin at the lateral surfaces. Thus, cell junctions must be partially disrupted to perturb the function of uvomorulin. We present a working model for the function of uvomorulin in the establishment of the epithelial occluding barrier.

Animals↗

PubMed2002

Chronic stress induces mast cell-dependent bacterial adherence and initiates mucosal inflammation in rat intestine.

BACKGROUND & AIMS: Chronic psychological stress is an important factor in relapses of intestinal disorders, but it remains unclear if stress can induce primary gut inflammation in a previously healthy host. METHODS: Mast cell-deficient (Ws/Ws) rats and wild-type control (+/+) rats were submitted to water avoidance stress or sham stress (1 h/day) for 10 consecutive days, as a model of ongoing life stress. RESULTS: Both rat groups had similar systemic responses to stress, as assessed by changes in weight, corticosterone levels, and defecation. In +/+ rats, chronic stress induced barrier dysfunction in the ileum and colon (increased macromolecular permeability and depletion of mucus) and ultrastructural changes in epithelial cells (enlarged mitochondria and presence of autophagosomes) associated with bacterial adhesion and penetration into enterocytes. Moreover, hyperplasia and activation of mast cells, infiltration of neutrophils and mononuclear cells, and increased myeloperoxidase (MPO) activity were documented in the mucosa. In intestine of Ws/Ws rats, epithelial function and morphology were unchanged by chronic stress, bacterial-epithelial cell interaction was not demonstrated, and there was no evidence of inflammatory cell infiltration. CONCLUSIONS: These findings suggest that chronic psychological stress can be an initiating factor in intestinal inflammation by impairing mucosal defenses against luminal bacteria and highlight the importance of mast cells in this process.

Animals↗

PubMed2005

Epithelial effects of proteinase-activated receptors in the gastrointestinal tract.

The intestinal epithelium plays a crucial role in providing a barrier between the external environment and the internal milieu of the body. A compromised mucosal barrier is characteristic of mucosal inflammation and is a key determinant of the development of intestinal diseases such as Crohn's disease and ulcerative colitis. The intestinal epithelium is regularly exposed to serine proteinases and this exposure is enhanced in numerous disease states. Thus, it is important to understand how proteinase-activated receptors (PARs), which are activated by serine proteinases, can affect intestinal epithelial function. This review surveys the data which demonstrate the wide distribution of PARs, particularly PAR-1 and PAR-2, in the gastrointestinal tract and accessory organs, focusing on the epithelium and those cells which communicate with the epithelium to affect its function. PARs have a role in regulating secretion by epithelia of the salivary glands, stomach, pancreas and intestine. In addition, PARs located on subepithelial nerves, fibroblasts and mast cells have important implications for epithelial function. Recent data outline the importance of the cellular site of PAR expression, as PARs expressed on epithelia may have effects that are countered by PARs expressed on other cell types. Finally, PARs and their ability to promote epithelial cell proliferation are discussed in terms of colon cancer.

Animals↗

PubMed1993

Effects of neuropeptides on neutrophil migration through noncellular and endothelial barriers.

BACKGROUND: Neuropeptides and neutrophils are postulated to be important immune effector molecules and cells, respectively, in a variety of lung inflammatory conditions. METHODS: We examined the effects of three lung neuropeptides, substance P, vasoactive intestinal peptide (VIP), and somatostatin and two relatively protease-resistant peptides, helodermin and sandostatin, on human neutrophil migration across 3 microns pore filters and human endothelial monolayers cultured on these filters. RESULTS: At concentrations of 1 to 10 mumol/L, substance P induced significant neutrophil migration that was dose-responsive and equivalent through endothelium and filters. Neither VIP, helodermin, somatostatin, nor sandostatin induced significant neutrophil migration through either barrier at doses of 10(-14) to 10(-5) mol/L. Because VIP and somatostatin have been reported to inhibit some inflammatory cell functions, we also examined their effects on chemoattractant-induced neutrophil migration. Pretreatment of neutrophils and/or endothelium with VIP or somatostatin at either 10(-5) or 10(-10) mol/L did not significantly inhibit formyl-methionyl-leucyl-phenylalanine-, leukotriene B4-, or platelet activating factor-induced neutrophil migration through naked filters or endothelium. Thus only substance P had significant effects on neutrophil chemotaxis. CONCLUSIONS: Substance P, but not VIP or somatostatin, may be important in directly influencing neutrophil migration across endothelium towards lung inflammatory sites. However, all three neuropeptides might still modulate neutrophil functions and lung inflammatory responses through effects on other lung cells.

Cell Line↗

PubMed1996

Interleukin-4 and interleukin-13 differentially regulate epithelial chloride secretion.

Intestinal epithelia are in intimate contact with subepithelial and intraepithelial lymphocytes. When stimulated, mucosal lymphocytes generate cytokines that act locally and influence functional aspects of many cell types. We have previously defined functional epithelial receptors for interferon-gamma, interleukin (IL)-4, and a recently described IL-4-like cytokine IL-13. In this study, we examine the ion transport properties of T84 cells, a crypt-like epithelial cell line, following exposure to IL-4 and IL-13. Basolateral exposure of epithelial monolayers to both IL-4 and IL-13 attenuated epithelial barrier function and increased paracellular flux of a dextran marker by greater than 65% in a dose- and time-dependent fashion. Stimulated Cl- secretion, as measured by epithelial short circuit current, however, was diminished only by IL-4 and not IL-13, demonstrating cytokine specificity in this epithelial function. Decreased Cl- secretion following IL-4 exposure was associated with diminished Cl- channel activity and IL-4 pretreatment of epithelia decreased expression of the cystic fibrosis transmembrane regulator. Finally, stimulated fluid transport across cultured epithelia was diminished following exposure to IL-4, but not IL-13. These results indicate that while post-receptor signaling events induced by IL-13 and IL-4 may be similar, end point function is cytokine-specific.

1-Methyl-3-isobutylxanthine↗

PubMed1997

CD95 (APO-1/Fas)-mediated apoptosis in colon epithelial cells: a possible role in ulcerative colitis.

BACKGROUND & AIMS: Ligation of CD95 (APO-1/Fas) by antibody or CD95 ligand (CD95L) induces apoptosis and, in some cell lines, growth. Normal colonic epithelial cells constitutively express CD95. The function of CD95 on colonocytes is unknown. The aim of this study was to elucidate the role of epithelial CD95 in the normal colon and in ulcerative colitis. METHODS: Intact colonic crypts were isolated, and the effects of CD95 ligation in vitro were studied. CD95L-expressing cells and apoptotic cells were detected in situ by RNA hybridization, immunohistochemistry, and DNA nick end labeling. RESULTS: On CD95 ligation, isolated colonic crypt cells underwent apoptosis within 4 hours. No growth-promoting effect was observed. In normal colon, CD95L expression was restricted to few mononuclear cells randomly scattered within the lamina propria. Therefore, the CD95-CD95L system is very unlikely to operate in the regeneration of the colonic epithelium. However, in ulcerative colitis, the number of interstitial CD95L+ cells and the frequency of apoptosis in both lamina propria and epithelium were increased considerably. Further, a focal association of subepithelial CD95L+ mononuclear cells and epithelial apoptosis was observed. CONCLUSIONS: In ulcerative colitis, soluble CD95L-mediated epithelial apoptosis may lead to a breakdown of the epithelial barrier function facilitating the invasion of pathogenic microorganisms.

Apoptosis↗

PubMed2003

[Early fracture fixation alleviates gut barrier function damage after multiple firearm injuries in pigs].

OBJECTIVE: To explore if early fracture fixation can alleviate gut barrier function damage caused by multiple firearm injuries in pigs. METHODS: Twelve healthy pigs were subjected to tangential fracture of parietal bone and comminuted fractures of bilateral femora (ISS >or= 16) due to 5.8 mm bullets shooting and these pigs were divided randomly into 2 groups. Control group (n = 6) were not treated at all. Fracture fixation Group (n = 6) were managed by immediate fracture fixation of bilateral femora with intramedullary nails. Plasma concentration of D-lactate, DAO and endotoxin (in portal vein) were detected at different intervals before and after trauma. The portal vein blood was cultured and the percentage of positive isolation was calculated. The concentration of DAO in small bowel was also detected 72 hours later after trauma. RESULTS: In control group, the plasma concentrations of D-lactate, DAO and endotoxin increased at early stage and kept high till 72 hours after trauma; the percentage of positive blood culture was 63.3%. In Group F, the levels of plasma D-lactate, DAO and endotoxin were also elevated at early stage (6 - 12 h), but declined significantly from 24 h or 48 h after trauma compared with control group (P < 0.05), and the percentage of positive blood culture was lower (30.0%, P < 0.05). The concentrations of DAO in small bowel decreased in both groups, but to a less extent in Group F. CONCLUSION: Bacterial and endotoxin translocation emerged with increasing gut permeability after multiple firearm injuries. The damage of gut barrier function could be alleviated and the chance of enterogenous infection could be by early fracture fixation after trauma.

Animals↗

PubMed1998

[Changes in permeability after ileoanal pouch anastomosis and in pouchitis].

The aim of the present study was to determine the changes in permeability and mucosal function after ileo-pouchanal anastomosis (IPAA) in patients with ulcerative colitis. We examined 24 patients (m: f = 15:9; Age = 35.2 +/- 12.5) prior to colectomy (pre IPAA), prior to closure of ileostomy (pre CIS), after closure of ileostomy (post CIS), in case of pouchitis and 5 controls. With a miniaturizised Ussing-chamber electrophysiological parameters of permeability and resorptive isotope-fluxes for mannitol were measured. Total resistance could be differenciated into epithelial and subepithelial resistance by using alternating current impedance measurements. Active Na(+)-glucose-Cotransport was measured by detection of the maximal short-curcuit-current under stepwise addition of glucose and active Cl(-)-secretion was measured by the increase in short-curcuit-current after stimulation with Theophillin and PGE2. Epithelial resistance of pouchitis was slightly raised towards controls but did not differ from the others. Subepithelial resistance post CIS and pouchitis was significantly increased versus controls and pre CIS (21.2 +/- 22.4 vs. 10.7 +/- 13.3 omega cm2) Whereas Cl-secretion of pouchitis was significantly reduced vs. post CIS and controls (38.6 vs. 120.9 +/- 113.9 microA cm-2). In the same way Na(+)-glucose Cotransport of pouchitis was significantly reduced vs. post CIS and controls(41.8 vs. 138.4 +/- 264.4 microA cm-2). Increasing subepithelial resistance post CIS and in pouchitis is a hint for an adaptive thickening of the subepitheal layer. Concerning the functional analysis pouchitis and terminal ileum prior to IPAA show a reduced secretion and resorption whereas the mucosal barrier towards Mannitol remains unchanged.

Biopsy↗

PubMed1999

Up-regulation of microsphere transport across the follicle-associated epithelium of Peyer's patch by exposure to Streptococcus pneumoniae R36a.

Transport of antigens through the follicle-associated epithelium (FAE) of Peyer's patch (PP) is the critical first step in the induction of mucosal immune responses. We have previously described that short-term exposure to Streptococcus pneumoniae R36a induced dramatic morphological alterations of the FAE in rabbit PP. These results prompted us to investigate whether the pneumococci-induced modifications were accompanied by enhanced ability of the FAE to transport antigens. We addressed this problem by evaluating the ability of the FAE to bind, internalize, and transport fluorescent polystyrene microparticles, highly specific to rabbit M cells, after exposure to S. pneumoniae. Quantitative study revealed a marked increase in the number of microspheres in PP tissues exposed to S. pneumoniae compared to tissues exposed to either phosphate-buffered saline or Escherichia coli DH5alpha as controls. No sign of bacterially induced damage to the epithelial barrier was observed. Further confocal microscopy analysis of the FAE surface showed that a significant increase in the number of cells that showed both morphological and functional features of M cells took place within pneumococci-treated PP tissues. These data provide the first direct evidence that the FAE-specific antigen sampling function may be manipulated to improve antigen and drug delivery to the intestinal immune system.

Animals↗

PubMed2006

Pregnane X receptor activation ameliorates DSS-induced inflammatory bowel disease via inhibition of NF-kappaB target gene expression.

Pregnane X receptor (PXR) expression was shown to be protective in inflammatory bowel disease (IBD). However, the mechanism by which PXR provides protection remains unclear. Wild-type and Pxr-null mice were treated with the PXR agonist pregnenolone-16alpha-carbonitrile or vehicle and administered 2.5% dextran sulfate sodium (DSS) in drinking water to induce IBD. Typical clinical symptoms were evaluated on a daily basis. In vivo intestinal permeability assays and proinflammatory cytokine analysis were performed. PXR agonist-treated mice were protected from DSS-induced colitis compared with vehicle-treated mice, as defined by body weight loss, diarrhea, rectal bleeding, colon length, and histology. Pregnenolone-16alpha-carbonitrile did not decrease the severity of IBD in Pxr-null mice. PXR agonist treatment did not increase epithelial barrier function but did decrease mRNA expression of several NF-kappaB target genes in a PXR-dependent manner. The present study clearly demonstrates a protective role for PXR agonist in DSS-induced IBD. The data suggest that PXR-mediated repression of NF-kappaB target genes in the colon is a critical mechanism by which PXR activation decreases the susceptibility of mice to DSS-induced IBD.

ATP-Binding Cassette Transporters↗