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Results for “Intestinal Barrier Function”

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PubMed2003

Association between the C3435T MDR1 gene polymorphism and susceptibility for ulcerative colitis.

BACKGROUND & AIMS: The human multidrug resistance 1 (MDR1) gene product P-glycoprotein is highly expressed in intestinal epithelial cells, where it constitutes a barrier against xenobiotics. The finding that mdr1a knockout mice develop a form of colitis that is similar to ulcerative colitis, which can be prevented by antibiotics, indicates a barrier function for P-glycoprotein against the invasion of bacteria or toxins. Because the MDR1 single nucleotide polymorphism C3435T is associated with lower intestinal P-glycoprotein expression, we tested whether this polymorphism predisposes to development of ulcerative colitis. METHODS: Allele frequencies and genotype distributions of the C3435T single nucleotide polymorphism were investigated in 149 patients with ulcerative colitis, 126 patients with Crohn's disease, and sex-matched healthy controls. RESULTS: Significantly increased frequencies of the 3435T allele and the 3435TT genotype were observed in patients with ulcerative colitis compared with controls (3435T: P = 0.049; odds ratio, 1.4; 95% confidence interval, 1.02-1.94; 3435TT: P = 0.045; odds ratio, 2.03; 95% confidence interval, 1.04-3.95). In contrast, frequencies of the T allele and the TT genotype were the same in patients with Crohn's disease as in controls (P = 0.66 and P = 0.59, respectively). In comparison to 998 non-sex-matched controls, the effect for the TT genotype in ulcerative colitis patients was more pronounced (P = 0.0055; odds ratio, 2.1). CONCLUSIONS: The higher frequency of the 3435TT genotype in patients with ulcerative colitis corroborates the findings from the mdr1a knockout mice. The results support the notion that P-glycoprotein plays a major role in the defense against intestinal bacteria or toxins. Impairment of barrier function in 3435TT subjects could render this genotype more susceptible to the development of ulcerative colitis.

Adolescent↗

PubMed2005

Resuscitation-induced gut edema and intestinal dysfunction.

BACKGROUND: Mesenteric venous hypertension and subsequent gut edema play a pivotal role in the development of intra-abdominal hypertension. Although gut edema is one cause of intra-abdominal hypertension, its impact on gut function is unknown. The purpose of this study was to create a model of acute hydrostatic gut edema and to evaluate its effect on gut motility and barrier function. METHODS: The first study, group A, evaluated the effect of gut edema on transit over time using 20 mL/kg 0.9% saline. The second study, group B, focused on the 12-hour time period using 80 mL/kg 0.9% saline. Rats were randomized to superior mesenteric vein partial occlusion (venous hypertension) or sham surgery. At 6, 12, and 24 hours, group A underwent intestinal transit and tissue water weight measurements. At 12 hours, group B underwent tissue water, transit, ileal permeability and resistance, lactate and myeloperoxidase activity, and mucosal injury measurements. RESULTS: Venous hypertension with fluid resuscitation caused acute hydrostatic gut edema, delayed intestinal transit, increased mucosal permeability to macromolecules, and decreased tissue resistance over time. Mucosal injury was minimal in mesenteric venous hypertension. CONCLUSION: Acute mesenteric venous hypertension and resuscitation-induced gut edema, in the absence of ischemia/reperfusion injury, is associated with delayed intestinal transit and altered gut barrier function.

Animals↗

PubMed1999

Ethanol-induced barrier dysfunction and its prevention by growth factors in human intestinal monolayers: evidence for oxidative and cytoskeletal mechanisms.

Exposure of intestinal mucosa to ethanol (EtOH) disrupts barrier function and growth factors [epidermal growth factor (EGF) and transforming growth factor-alpha (TGF-alpha)] are protective, but the mechanisms remain obscure. Accordingly, we sought to determine whether the molecular mechanism of EtOH-induced intestinal barrier dysfunction involves oxidative stress and disassembly of microtubules and whether the mechanism of protection by EGF or TGF-alpha involves prevention of these alterations. To this end, human colonic (Caco-2) monolayers were exposed to 0 to 15% EtOH with or without pretreatment with EGF or TGF-alpha (10 ng/ml) or with oxidative or cytoskeletal modulators. Effects on cell viability, barrier function, tubulin (microtubules), and oxidative stress were then determined. Cells were also processed for immunoblots of polymerized tubulin (S2; index of stability) and the monomeric tubulin (S1; index of disruption). EtOH dose-dependently decreased the stable S2 polymerized tubulin and concomitantly increased measures of oxidative stress, including oxidation and nitration of tubulin, fluorescence of dichlorofluorescein, and inducible nitric oxide synthase activity. EtOH also dose-dependently disrupted barrier function and extensively damaged microtubules, and these effects were prevented by pretreatment with antioxidant scavengers: L-cysteine, superoxide dismutase, and L-N(6)-1-iminoethyl-lysine (an inducible nitric oxide synthase inhibitor). In monolayers exposed to EtOH, pretreatment with EGF or TGF-alpha prevented the oxidation and nitration of tubulin, increases in the levels of the unstable S1 tubulin, disruption of microtubules, and barrier dysfunction. A microtubule stabilizer (paclitaxel,Taxol) mimicked, in part, the effects of EGF and TGF-alpha, whereas a microtubule disruptive drug (colchicine) prevented the protective effects of these growth factors. We concluded that mucosal barrier dysfunction induced by EtOH involves oxidative stress, which causes the disassembly of the microtubule cytoskeleton. Protection by EGF and TGF-alpha involves the prevention of these EtOH-induced alterations in microtubules.

Antioxidants↗

PubMed1990

Maintenance of the macromolecular barrier at cell extrusion sites in intestinal epithelium: physiological rearrangement of tight junctions.

All epithelia slough dying cells but the consequences of this physiological process to epithelial barrier function is unknown. In mammalian small intestine absorptive cells are known to migrate from the villus base to the villus tip from which they slough. These villus tip extrusion zones are often envisioned as sites at which macromolecules could leak across the epithelium. However, only trace amounts of macromolecules cross this epithelium even though, based on known epithelial turnover rates, extrusion events occur millions of times daily. Here, we examine the characteristics of the epithelial barrier to macromolecular permeation at villus tip extrusion zones in rats and hamsters. Freeze-fracture, light and electron microscope studies reveal that extruding cells do not leave transient holes behind as they lift from the epithelium. Rather, as cells extrude, processes of adjacent cells extend under them. Moreover, tight junction elements proliferate between extruding cells and their neighbors and appear to move down the lateral margin of the extruding cell as it extends into the lumen. These observations suggest that newly formed junctional elements "zipper" the epithelium closed as extrusion proceeds thus preventing epithelial discontinuities from occurring. Correlative in vivo perfusion experiments using horseradish peroxidase as a macromolecular-tracer show that the above described dynamic alterations in tight junctions at extrusion sites are generally sufficient to prevent transepithelial leaks of macromolecules.

Animals↗

PubMed2003

Higher concentrations of interferon-gamma enhances uptake and transport of dietary antigens by human intestinal cells: a study using cultured Caco-2 cells.

Besides functioning as a mucosal barrier and transporting nutrients, intestinal epithelial cells (IECs) also serve as antigen-presenting cells (APCs). Modification of protein antigens by proteolysis is one of the principal steps in antigen presentation to Th cells. We used a Caco-2 intestinal epithelial cell line to investigate the transepithelial transport of the dietary antigen, ovalbumin (OVA). We also examined the effects of the proinflammatory cytokine interferon-gamma (IFN-gamma) on the antigen transport process in Caco-2 cell layers. Caco-2 cell layers transferred both intact and degraded OVA from the mucosal to the serosal side. IFN-gamma stimulated OVA transport and most of the transported OVA in such cells were degraded. We also examined OVA uptake by Caco-2 cells using immunohistochemical means. Caco-2 cells incorporated OVA in a time-dependent manner and IFN-gamma significantly enhanced antigen internalization. Flow cytometry also demonstrated that IFN-gamma elevated the internalization of FITC-OVA. We also determined the effects of low and high concentrations of IFN-gamma on mucosal permeability and internalization of FITC-OVA. Although both 10 and 50 ng/mL IFN-gamma stimulated mucosal permeability to the same extent, more FITC-OVA was internalized by Caco-2 cells incubated with 50 than with 10 ng/mL IFN-gamma. These results suggest that the effects of IFN-gamma on mucosal permeability and the internalization of antigens by intestinal epithelial cells are brought about by different mechanisms. Therefore, higher concentrations of IFN-gamma stimulate the uptake, processing, and transport of dietary antigens by IECs.

Antigen Presentation↗

PubMed1994

[An experimental study of the mechanism of shock-induced enterogenic infection after long-term standard total parenteral nutrition].

In this study, gnotobiotic rats were subjected to total parenteral nutrition (TPN) and subsequent hemorrhagic shock to study the mechanism of enterogenic infection in these circumstances. (1) Long-term (8-12 days) TPN induced impairment of gut barrier function, evidenced by atrophy of intestinal mucosa, significant decrease in diamine oxidase activity of intestinal mucosa and blood, and marked micro-ecologic imbalance of the intestinal mucosa flora with dominant growth of aerobes and relative decrease in anaerobes. The degree of mucosal damage were proportional to the duration of TPN. (2) In TPN+shock groups, further damage was found in the mucosa, with a large number of invading gram-negative organisms and a significant decrease in DAO activity as compared to that with TPN only groups. These changes were significantly correlated with enhanced bacterial translocation, elevation of LPS and MDA levels in the plasma. These findings suggested that long term TPN impairing gut barrier function, precipitated posttraumatic gut barrier failure. The determination of plasma DAO activity may help in the early diagnosis of gut injury during TPN and after trauma.

Actinomycetales Infections↗

PubMed1987

Structural and functional maturation of rat gastrointestinal barrier with thyroxine.

It has been noted that the closure of the intestinal barrier to immunoglobulins is a normal maturational process in the rat. It has also been noted that the microvillus membrane (MVM) of newborn animals differs from adult MVM. The purpose of this study is to document whether thyroid hormone can induce closure in vivo in the rat and to relate this effect of thyroxine to the structural and functional maturation of the intestinal MVM. To assess closure, 2-wk-old rats were fed a rat immunoglobulin G (IgG), and serum antibody binding activity was measured 4 h later. The antibody binding activity of treated animals (T) was 1.5-2 times less than that of controls (C) (P less than 0.001), indicating that thyroxine stimulates closure. The MVM similarly showed signs of maturation. Structural maturation was demonstrated by the lower fluidity of the thyroid-treated animals' membranes. Under the influence of thyroxine, the number of receptors on the MVM for IgG had decreased [2.8 X 10(-7) M (C) vs. 1.7 X 10(-7) M (T)], while the Ka remained the same, demonstrating the functional maturation of the MVM. In conclusion, thyroid hormone can induce both structural and functional maturation of the intestinal MVM and can enhance the intestinal mucosal barrier by decreasing the penetration of antibodies.

Animals↗

PubMed2003

In vivo influence of nicotine on human basal and NSAID-induced gut barrier function.

BACKGROUND: Smoking reduces the non-steroidal anti-inflammatory drug (NSAID)-induced small intestinal permeability increase in healthy people. It also affects inflammatory bowel disease that is associated with a disturbed gut barrier function. To assess the role of nicotine on barrier function, its influence on basal and NSAID-induced intestinal permeability was studied in healthy volunteers. METHODS: Thirty-one healthy non-smoker subjects performed permeability tests with 51Cr-EDTA and sugar markers (sucrose, lactulose, mannitol, sucralose) before and during 2 weeks of nicotine patch application, and with and without indomethacin intake, respectively. Since smoking has been described as affecting motility, transit measurements were also done with the sodium[13C]-octanoate and lactose-[13C]-ureide breath tests before and during nicotine exposure. Correlations between permeability markers were checked and the influence of gastrointestinal transit was assessed. RESULTS: Nicotine did not affect barrier function in vivo, nor gastric emptying, small-bowel transit time or orocaecal transit. 51Cr-EDTA and lactulose correlated in basal 0-6 h permeability testing (r = 0.529, P < 0.0001), as did 6-24 h excretion of 51Cr-EDTA and sucralose (r = 0.474, P < 0.001); 97% and 90% of the subjects had a permeability increase after indomethacin intake for 0-6 h and 6-24 h excretion of Cr-EDTA, respectively. This population proportion is 63% for lactulose/mannitol and 83% for sucralose. CONCLUSIONS: Short-term exposure to nicotine does not alter normal basal or NSAID-induced gut barrier function or transit. 51Cr-EDTA and the respective sugar markers correlate well in in vivo permeability testing in healthy humans. The radioactive test detects more NSAID-induced permeability increase than does the lactulose/mannitol ratio permeability test.

Adult↗

PubMed2002

A coculture model mimicking the intestinal mucosa reveals a regulatory role for myofibroblasts in immune-mediated barrier disruption.

The pathogenesis of Crohn's disease involves a mucosal inflammatory response affecting the barrier function of the gut. Myofibroblasts directly underlining the intestinal epithelium may have a regulatory role in immune-mediated barrier disruption. A coculture system of T84 epithelial and CCD-18Co myofibroblasts was established in order to mimic the in situ spatial interactions between these cell types and to evaluate their role in barrier: integrity. Lamina propria mononuclear cells (LPMC) were introduced in co- and monocultures. Effects of immune cells on barrier integrity was determined by measuring resistance and permeability for macromolecules. Introduction of LPMC in both culture systems caused a time-dependent decrease in barrier integrity. This was found to be less pronounced in cocultures indicating a regulatory role for mesenchymal cells. The effects were also found to depend on the route of LPMC stimulation. Additional analyses suggested that the regulatory role of myofibroblasts in barrier integrity involves production of growth factors.

Cell Line↗

PubMed2000

[Effect of abdominal lavage with Chinese drugs on bacteria translocation in acute hemorrhagic necrotizing pancreatitis in rats].

OBJECTIVE: To investigate the effect of different abdominal lavage fluid on bacterial translocation in acute hemorrhagic necrotizing pancreatitis (AHNP) of rat model. METHODS: One hundred and sixty Wistar rats were randomly divided into the control group, AHNP group, antibiotics group and Chinese drugs group. The treated group were treated with intraperitoneal lavage for 72 hours. The peritoneal fluid and blood samples were collected for bacterial culture. Pancreas were examined histopathologically. RESULTS: In Chinese drugs group, the pathologic damage in pancreas were milder than that of AHNP group, and as compared with AHNP group, the bacterial positive rates of blood and peritoneal lavage fluid culture were reduced from 80% to 40% and 90% to 40% respectively. CONCLUSION: AHNP impaired the gut barrier function which led to bacterial translocation from the gut to other organs. It plays an important role in intestinal infection secondary to AHNP. Abdominal lavage with Chinese drugs is effective in preventing intestinal bacterial translocation, it showed its protection on gut barrier function by alleviating the damage of intestinal mucosa and pancreatitis.

Animals↗

PubMed1994

F-actin differentially alters epithelial transport and barrier function.

Vectorial ion transport and barrier function are two fundamental and defining properties of all epithelial cells. To define the role of F-actin in these dual properties, we studied the effects of two probes of cytoskeletal function on the well-differentiated human intestinal epithelial cell line T84: cytochalasin D, a fungal metabolite widely used to disrupt microfilament function by an uncertain mechanism, and phalloidin, a more specific agent which binds and stabilizes F-actin with high affinity, thus preventing actin depolymerization. T84 cells grown on collagen-coated permeable supports were studied by dual voltage-current clamping; transepithelial resistance to passive ion flow (R, an indirect measure of junctional integrity) and short-circuit current (a measure of net electrogenic ion transport response to the adenylate cyclase activator forskolin was preserved. In contrast, stabilization of F-actin by incubation with phalloidin for up to 24 hr produced no change in R but caused a profound inhibition of cAMP-stimulated short-circuit current. Thus, cytochalasin D was found to perturb barrier but not transport function of T84 monolayers; conversely, stabilization of F-actin by phalloidin was found not to affect barrier function but markedly attenuated electrogenic ion transport. The results suggest that the dual properties of barrier function and ion transport in intestinal epithelia may be differentially influenced by dynamic alterations in F-actin.

Actins↗

PubMed1996

[An experimental study on injury of intestinal immuno-barrier in rat after scald].

A dynamic observation on injury of intestinal immuno-barrier in scalded rat was performed to investigate the relationship between the injury of intestinal immuno-barrier and bacterial translocation. After 40% TBSA third degree scald, a decrease of IgA in intestinal content and the number of CD3+ and CD4+ T lymphocyte, and reduction of IgA coat rate of intestinal bacteria were observed. At the same time, an increase in the incidence of bacterial translocation was detected. The results indicated that intestinal immuno-barrier was damaged and its protective function was weakened after an extensive thermal injury, and it suggested that the injury of intestinal immuno-barrier might play an important role on the development of postburn bacterial translocation and postburn sepsis.

Animals↗

PubMed1994

[Preserving intestinal function after severe burn injury].

To study the changes of the bowel-barrier function and its preservation, we developed a new animal model. A specially bred miniswine (Guizhou species) was used with multiple catheterizations for sampling different blood from portal, inferior mesenteric as will as jugular (central) veins. The animals were sustained with 30% III burns of TBSA 7 days after catheterization and divided randomly into early feeding (EF) group, given a complete diet beginning from 2 hours postburn (n = 6) and delayed feeding (DF) group, given the same diet initiating on 4 days postburn (n = 6). The results indicated that the bowel-barrier function was weakened significantly early postburn so that the translocation of both endotoxin and bacteria from the gut to portal vein was evidently increased. However, improving the intestinal mucosa ischemia, preserving mucosal mass and maintaining bowel-microecological balance through early enteral feeding, as revealed in this study, could enhance the barrier function, and the translocation of bacteria and endotoxin would be thus decreased to some extent.

Animals↗

PubMed1998

Increased intestinal permeability and altered mucosal immunity in cholestatic jaundice.

OBJECTIVE: To examine the effects of cholestatic jaundice on gut barrier function. SUMMARY BACKGROUND DATA: Gut barrier failure occurs in animal models of jaundice. In humans, the presence of endotoxemia indirectly implicates failure of this host defense, but this has not previously been investigated in jaundiced patients. METHODS: Twenty-seven patients with extrahepatic obstructive jaundice and 27 nonicteric subjects were studied. Intestinal permeability was measured using the lactulose-mannitol test. Small intestinal morphology and the presence of mucosal immunologic activation were examined in endoscopic biopsies of the second part of the duodenum. Systemic antiendotoxin core IgG antibodies and serum interleukin-6 and C-reactive protein were also quantified. Intestinal permeability was remeasured in 9 patients 5 weeks after internal biliary drainage. RESULTS: The median lactulose-mannitol ratio was significantly increased in the jaundiced patients. This was accompanied by upregulation of HLA-DR expression on enterocytes and gut-associated lymphoid tissue, suggesting immune activation. A significant increase in the acute phase response and circulating antiendotoxin core antibodies was also observed in the jaundiced patients. After internal biliary drainage, intestinal permeability returned toward normal levels. CONCLUSIONS: A reversible impairment in gut barrier function occurs in patients with cholestatic jaundice. Increased intestinal permeability is associated with local immune cell and enterocyte activation. In view of the role of gut defenses in the modern paradigm of sepsis, these data may directly identify an important underlying mechanism contributing to the high risk of sepsis in jaundiced patients.

Acute-Phase Reaction↗

PubMed2006

Short-term effects of depleted uranium on immune status in rat intestine.

In the event of ingestion, the digestive tract is the first biological system exposed to depleted uranium (DU) intake via the intestinal lumen. However, little research has addressed the biological consequences of a contamination with depleted uranium on intestinal properties such as the barrier function and/or the immune status of this tissue. The aim of this study was to determine if the ingestion of depleted uranium led to changes in the gut immune system of the intestine. The experiments were performed at 1 and 3 d following a per os administration of DU to rats at sublethal dose (204 mg/kg). Several parameters referring to the immune status, such as gene and protein expressions of cytokines and chemokines, and localization and density of immune cell populations, were assessed in the intestine. In addition, the overall toxicity of DU on the small intestine was estimated in this study, with histological appearance, proliferation rate, differentiation pattern, and apoptosis process. Firstly, the results of this study indicated that DU was not toxic for the intestine, as measured by the proliferation, differentiation, and apoptosis processes. Concerning the immune properties of the intestine, the ingestion of depleted uranium induced some changes in the production of chemokines and in the expression of cytokines. A diminished production of monocyte chemoattractant protein-1 (MCP-1) was noted at 1 day post exposure. At 3 d, the increased gene expression of interferon gamma (IFNgamma) was associated with an enhanced mRNA level of Fas ligand, suggesting an activation of the apoptosis pathway. However, no increased apoptotic cells were observed at 3 d in the contaminated animals. There were no changes in the localization and density of neutrophils, helper T lymphocytes, and cytotoxic T lymphocytes after DU administration. In conclusion, these results suggest that depleted uranium is not toxic for the intestine after acute exposure. Nevertheless, DU seems to modulate the expression and/or production of cytokines (IFNgamma) and chemokines (MCP-1) in the intestine. Further experiments need to be performed to determine if a chronic contamination at low dose leads in the long term to modifications of cytokines/chemokines patterns, and to subsequent changes in immune response of the intestine.

Animals↗

PubMed1996

Enhanced absorption of macromolecules. A secondary factor in Crohn's disease.

We explored the function of the intestine's mucosal barrier to foreign antigen entry in Crohn's disease. Macroscopically and microscopically uninvolved areas of the small intestines of patients with Crohn's disease were examined. We studied 27 endoscopic biopsy samples from 17 patients with Crohn's disease and 14 samples from nine controls. The absorption and degradation of horseradish peroxidase (molecular weight 40,000 Da) were studied in Ussing chambers. The absorption of intact horseradish peroxidase was significantly increased in patients with moderate or severe Crohn's disease: 271 (95% confidence interval 119-616) ng/hr/cm2, but not in those with slight disease activity: 42 (18-98), compared with controls: 45 (32-64); F = 10.90, P = 0.0002. The transport rates of degraded horseradish peroxidase were comparable in the Crohn's disease samples and controls. Our results indicate that enhanced absorption of macromolecules is associated with clinical activation of Crohn's disease, and impairment of the mucosal barrier function is a secondary phenomenon in Crohn's disease.

Adult↗

PubMed1995

Ammonia inhibits cAMP-regulated intestinal Cl- transport. Asymmetric effects of apical and basolateral exposure and implications for epithelial barrier function.

The colon, unlike most organs, is normally exposed to high concentrations of ammonia, a weak base which exerts profound and diverse biological effects on mammalian cells. The impact of ammonia on intestinal cell function is largely unknown despite its concentration of 4-70 mM in the colonic lumen. The human intestinal epithelial cell line T84 was used to model electrogenic Cl- secretion, the transport event which hydrates mucosal surfaces and accounts for secretory diarrhea. Transepithelial transport and isotopic flux analysis indicated that physiologically-relevant concentrations of ammonia (as NH4Cl) markedly inhibit cyclic nucleotide-regulated Cl- secretion but not the response to the Ca2+ agonist carbachol. Inhibition by ammonia was 25-fold more potent with basolateral compared to apical exposure. Ion substitution indicated that the effect of NH4Cl was not due to altered cation composition or membrane potential. The site of action of ammonia is distal to cAMP generation and is not due simply to cytoplasmic alkalization. The results support a novel role for ammonia as an inhibitory modulator of intestinal epithelial Cl- secretion. Secretory responsiveness may be dampened in pathological conditions associated with increased mucosal permeability due to enhanced access of lumenal ammonia to the basolateral epithelial compartment.

Ammonia↗

PubMed2003

Prolonged interferon-gamma exposure decreases ion transport, NKCC1, and Na+-K+-ATPase expression in human intestinal xenografts in vivo.

IFN-gamma is elevated in intestinal inflammation and alters barrier and transport functions in human colonic epithelial cell lines, but its effects on normal human small intestinal epithelium in vivo are poorly defined. We investigated effects of prolonged IFN-gamma exposure on ion transport and expression of transporters by using human fetal small intestinal xenografts. Xenograft-bearing mice were injected with IFN-gamma, and 24 h later xenografts were harvested and mounted in Ussing chambers. Baseline potential difference (PD) was not affected by IFN-gamma treatment. However, conductance was enhanced and agonist-stimulated ion transport was decreased. IFN-gamma also decreased expression of the Na+-K+-2Cl- cotransporter and the alpha-subunit of Na+-K+-ATPase compared with controls, whereas levels of the calcium-activated Cl- channel and CFTR were unaltered. Thus prolonged exposure to IFN-gamma leads to decreased ion secretion due, in part, to decreased ion transporter levels. These findings demonstrate the implications of elevated IFN-gamma levels in human small intestine and validate the human intestinal xenograft as a model to study chronic effects of physiologically relevant stimuli.

Animals↗