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PubMed2004

Intestinal barrier function and secretion in methotrexate-induced rat intestinal mucositis.

Chemotherapy-induced mucositis is an important dose-limiting and costly side effect for which there is no definitive prophylaxis or treatment. This is due in part to the lack of understanding of its pathophysiology and impact on intestinal function. The objectives of this study were to investigate the small intestine barrier function and electrolyte and water transport in an experimental model of methotrexate-induced mucositis, and to correlate these alterations with histological damage. Wistar rats were treated with methotrexate (1.5-3.5 mg/kg) for 3 days to induce mucositis. Intestinal permeability was measured by the urinary excretion rate of lactulose and mannitol following administration by gavage. Intestinal perfusion was performed in vivo for evaluation of water and electrolyte transports. Methotrexate-treated rats lost a significant amount of weight and presented a marked reduction in food intake. Methotrexate induced significant and dose-dependent villous atrophy and elongation of crypts in duodenum, jejunum, and ileum. Methotrexate also induced an increase in sodium and potassium secretion and an important reduction of the mucosa absorptive surface area, shown by the decrease in the mannitol excretion ratio. In conclusion, methotrexate caused major changes in small bowel function by disrupting intestinal permeability and inducing electrolyte secretion in parallel with substantial histological damage.

Animals↗
PubMed2000

Oxidant-induced intestinal barrier disruption and its prevention by growth factors in a human colonic cell line: role of the microtubule cytoskeleton.

Reactive oxygen metabolites (ROM) are increased in the inflamed mucosa of inflammatory bowel disease (IBD) and may contribute to loss of intestinal barrier function in this disorder. Growth factors (GF) are protective. But the mechanisms of disruption and protection remain elusive. In the present investigation, we hypothesized that the microtubules (a critical cytoskeletal element) play a key role in the molecular mechanism of intestinal barrier dysfunction induced by ROM and in GF-mediated protection. Utilizing monolayers of a human colonic cell line (Caco-2), we evaluated the effects of ROM (H(2)O(2) or HOCl), in the presence or absence of GF (epidermal growth factor [EGF]; transforming growth factor-alpha [TGF-alpha]), on intestinal barrier function, tubulin (microtubule structural protein), and microtubule stability. Monolayers were also processed for two highly sensitive western immunoblots: fractionated polymerized tubulin (S2; an index of stability); monomeric tubulin (S1; an index of disruption) to detect the oxidation and disassembly/assembly of tubulin. ROM exposure led to a significant increase in the oxidation of tubulin, decrease in the stable S2 polymerized tubulin, and increase in the unstable S1 monomeric tubulin. In concert, each ROM in a dose dependent manner damaged the microtubule cytoskeleton and disrupted barrier function. GF pretreatment not only increased the S2 stable tubulin and decreased tubulin oxidation but also, concomitantly, prevented the disruption of microtubules and loss of barrier function in monolayers exposed to ROM. Antibody against the GF-receptor and inhibitors of GF-receptor tyrosine kinase abolished GF protection, indicating the involvement of epidermal growth factor receptor (EGFR) signaling pathway. As predicted, colchicine, an inhibitor of microtubule assembly, caused barrier dysfunction and prevented GF protection whereas taxol, a microtubule-stabilizing agent, mimicked the protective effects of GF. Thus, organization and stability of the microtubule cytoskeleton appears to be critical to both oxidant-induced mucosal barrier dysfunction and protection of intestinal barrier mediated by GF. Therefore, microtubules may be useful targets for development of drugs for the treatment of IBD.

Caco-2 Cells↗
PubMed2004

[Experimental study on protecting intestinal barrier function of Huoxiang Zhengqi soft capsule].

OBJECTIVE: To study the effect of Huoxiang Zhengqi soft capsule on protecting intestinal barrier. METHOD: Lower limb ischemic reperfusion model was induced in Wistar rats. The Chinese medicine groups were administered orally with Huoxiang Zhengqi soft capsule before inoculation respectively. The small intestinal histopathology and ultrastructural of rats were observed with optical microscope and electronic microscope respectively. Mucus was observed under AB-PAS staining, mast cells were studied under toluidine blue staining, and serum NO was determined. RESULT: After Lower limb ischemic reperfusion, the intestinal barrier function was severely damaged. Huoxiang Zhengqi soft capsule could significantly reduce the levels of the serum NO (P < 0.01). CONCLUSION: Huoxiang Zhengqi soft capsule has apparent protective effect on the intestinal barrier function in lower limb ischemic reperfusion rats.

Animals↗
PubMed1983

Experimental diabetes and intestinal barriers to absorption.

The unstirred water layer (UWL) and the brush-border membrane represent the major barriers to intestinal absorption. Enhanced uptake of several nutrients has been described in diabetes mellitus, and this study was undertaken in the rat to define whether these absorptive changes are due to alterations in the characteristics of these barriers. Using in vitro techniques the effective resistance of UWL was measured with lauryl alcohol, the rate of uptake (Jd) of which is limited by diffusion across the UWL. At all rates of stirring of the bulk phase, the effective resistance of UWL was less in diabetic than control rats. The Jd of a homologous series of saturated fatty acids (4:0-18:0) and cholesterol was higher than disks of intestine of diabetic than control intestine; this enhanced uptake of lipid could not be demonstrated using intestinal biopsies. The change in incremental free energy of transfer of fatty acid uptake into disks was higher in diabetic than control animals after correction for UWL effects. After correction for UWL, the Michaelis constant for Jd of D-glucose was similar in diabetic and control jejunum, and the greater Jd of glucose in diabetics was due to a higher maximal transport rate (Jmd) and a higher passive permeability coefficient. It is concluded that the enhanced uptake of glucose, fatty acids, fatty alcohols, and cholesterol into diabetic intestine is due to a reduction in the effective resistance of the UWL, an increase in the passive permeability properties of the membrane, and a rise in the Jmd for D-glucose.

Animals↗
PubMed2000

Stress-induced decrease of the intestinal barrier function. The role of muscarinic receptor activation.

Recently the breakdown of the barrier function of the intestinal epithelium after application of an experimental psychological and physical stress protocol in rats has been observed. Not only did smaller molecules pass from the luminal to the serosal side, but so also did larger proteins with the dimensions of luminal antigens and toxins. The increased permeability for macromolecules is primarily due to a decrease of the tightness of the zonula occludens, but an increased endocytotic uptake indicates that transcytosis is increased also. From studies of model systems it can be concluded that activation of the intracellular protein kinase C route by muscarinic receptor activation or histamine receptor activation can be one of the underlying cellular pathways. The physical pathway relaying the stress from the brain to the intestinal tract appears to be the parasympathetic branch of the autonomic nervous system. The difference in reaction of different strains suggests that coping style is an important determinant of the response of the intestinal barrier to stress.

Animals↗
PubMedDate not supplied

[Effect of diet therapy on the state of the intestinal barrier in digestive organ diseases].

The effect of diets with varying amount of protein (135 and 160 g) on the intestinal barrier was studied in patients with the inadequate absorption syndrome of different etiology (chronic enterocolitis, the postgastroresection syndrome, chronic colitis). The data obtained indicate that in spite of the progress attained in the care of such patients at the present time, they show disturbed permeability of the intestinal barrier, determined by the passive hemagglutination test (PHAT) with diverse fractions of milk protein. With the postgastroresection syndrome, the abnormalities in the intestinal barrier arise less frequently, are less pronounced and more amenable by therapy as compared to patients with chronic enterocolitis. However, the condition of the small intestine should be taken into consideration in making dietetic recommendations for the patients suffering from the above diseases. The clinical findings and PHAT dynamics indicate that inclusion into the diet of over 135 g protein is not desirable.

Antibodies↗
PubMed1989

Bacterial chemotactic oligopeptides and the intestinal mucosal barrier.

Intestinal absorption and enterohepatic circulation of N-formyl-methionyl-leucyl-125I-tyrosine, a bioactive synthetic analog of the bacterial chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine has been investigated in the rat. In ileum and proximal and distal colon, dithiothreitol, which increases mucosal permeability, increased peptide absorption and biliary recovery fourfold, 70-fold, and 20-fold over control values, respectively. When dithiothreitol was combined with d-l-benzyl succinate, a potent inhibitor of intestinal carboxypeptidase, absorption and biliary recovery from ileal loops increased markedly to 40-fold over control, whereas there was no further increase in absorption from colon loops. There was a strong correlation between biliary N-formyl-methionyl-leucyl-125I-tyrosine recovery and intestinal absorption of 51Cr-ethylenediaminetetraacetate, a marker of passive mucosal permeability (r = 0.97). We conclude that in the ileum both enzymic degradation and restricted mucosal permeability contribute to the intestinal barrier to luminal bacterial formyl oligopeptides. In the colon, however, enzymic mechanisms are less active and restricted mucosal permeability is the major factor. Abnormalities of the intestinal mucosal barrier to proinflammatory bacterial peptides could play a role in inflammatory disorders of the gut.

Animals↗
PubMed1998

[Effect of a bioactive food supplement from selenium enriched baker's yeast autolysate on the status of the intestinal barrier in rats with anaphylaxis].

Rat's intestinal barrier permeability disturbed in consequence of intestinal anaphylaxis reaction was almost completely normalized in animals fed with baker's yeast autolysate "Vitasil" enriched with selenium on a level of 3 mg Se/day during 29 days. These rats showed in comparison to Se-unsupplemented animals a significant elevation of Se level in red blood cells and plasma together with a decrease of intestinal mucosal TCA-soluble thiol compounds. Urinary Se excretion was significantly elevated in comparison to unsensitized rats both in Se-supplemented and unsupplemented animals with anaphylaxis. It's concluded that "Se-Vitasil" may be successfully used in antioxidative therapy of food allergy, malabsorption, inflammatory bowel diseases and intestinal infection.

Anaphylaxis↗
PubMed2004

Intestinal barrier damage caused by trauma and lipopolysaccharide.

AIM: To investigate the intestinal barrier function damage induced by trauma and infection in rats. METHODS: Experimental models of surgical trauma and infection were established in rats. Adult Sprague-Dawley rats were divided into 4 groups: control group (n = 8), EN group (n = 10), PN group (n = 9) and Sep group (n = 8). The rats in PN and Sep groups were made into PN models that received isonitrogenous, isocaloric and isovolumic TPN solution during the 7-d period. Rats in EN and Sep groups received laparotomy and cervical catheterization on day 1 and received lipopolysaccharide injection intraperitoneally on d 7. On the 7(th) day all the animals were gavaged with lactulose and mannitol to test the intestinal permeability. Twenty-four hours later samples were collected and examined. RESULTS: The inflammatory responses became gradually aggravated from EN group to Sep group. The mucosal structure of small intestine was markedly impaired in PN and Sep groups. There was a low response in IgA level in Sep group when compared with that of EN group. Lipopolysaccharide injection also increased the nitric oxide levels in the plasma of the rats. The intestinal permeability and bacterial translocation increased significantly in Sep group compared with that of control group. CONCLUSION: One wk of parenteral nutrition causes an atrophy of the intestinal mucosa and results in a moderate inflammatory reaction in the rats. Endotoxemia aggravates the inflammatory responses that caused by laparotomy plus TPN, increases the production of nitric oxide in the body, and damages the intestinal barrier function.

Animals↗
PubMed1980

Intestinal barrier to large particulates in mice.

Intestinal barrier function in mice was assessed after acute or chronic oral administration of 15.8- and 5.7-micron synthetic spherical particles. The results failed to confirm previous reports that ingested particles rapidly appear in blood. Furthermore, 15.8-micron particles did not accumulate in intestinal Peyer's patches, mesenteric lymph nodes, or other organs of the reticuloendothelial system, even after the maximum dosage of 8 X 10(6) particles per day for 60 d. However, the 5.7-micron particles were demonstrated in Peyer's patches, mesenteric lymph nodes, and lungs after the maximum dosage of 4.5 X 10(8) particles per day for 60 d. At 77 d after the termination of ingestion, 5.7-micron particles were still present in these tissues. The 5.7-micron particles were not found in spleen; retention in liver was equivocal. The site of uptake of particles capable of penetrating the intestinal mucosa appears to be the Peyer's patches. It is suggested that most absorbed particles are sequestered in Peyer's patch macrophages. Particles that escape sequestration are transported by lymph rather than by portal blood. The findings indicate that hazards associated with intestinal uptake of large (> 5 micron) particulates exist, but that the frequency of such penetration is still unclear.

Animals↗
PubMed2006

Enterocyte TLR4 mediates phagocytosis and translocation of bacteria across the intestinal barrier.

Translocation of bacteria across the intestinal barrier is important in the pathogenesis of systemic sepsis, although the mechanisms by which bacterial translocation occurs remain largely unknown. We hypothesized that bacterial translocation across the intact barrier occurs after internalization of the bacteria by enterocytes in a process resembling phagocytosis and that TLR4 is required for this process. We now show that FcgammaRIIa-transfected enterocytes can internalize IgG-opsonized erythrocytes into actin-rich cups, confirming that these enterocytes have the molecular machinery required for phagocytosis. We further show that enterocytes can internalize Escherichia coli into phagosomes, that the bacteria remain viable intracellularly, and that TLR4 is required for this process to occur. TLR4 signaling was found to be necessary and sufficient for phagocytosis by epithelial cells, because IEC-6 intestinal epithelial cells were able to internalize LPS-coated, but not uncoated, latex particles and because MD2/TLR4-transfected human endothelial kidney (HEK)-293 cells acquired the capacity to internalize E. coli, whereas nontransfected HEK-293 cells and HEK-293 cells transfected with dominant-negative TLR4 bearing a P712H mutation did not. LPS did not induce membrane ruffling or macropinocytosis in enterocytes, excluding their role in bacterial internalization. Strikingly, the internalization of Gram-negative bacteria into enterocytes in vivo and the translocation of bacteria across the intestinal epithelium to mesenteric lymph nodes were significantly greater in wild-type mice as compared with mice having mutations in TLR4. These data suggest a novel mechanism by which bacterial translocation occurs and suggest a critical role for TLR4 in the phagocytosis of bacteria by enterocytes in this process.

Animals↗
PubMed1999

Intestinal barrier function and cow's milk sensitization in guinea pigs fed milk or fermented milk.

BACKGROUND: The respective effect of milk and fermented milks on intestinal barrier capacity and on sensitization to beta-lactoglobulin was studied using a guinea pig model of cow's milk allergy. METHODS: Guinea pigs were fed a control diet or the same diet supplemented with milk, fermented milk (Streptococcus thermophilus and Bifidobacterium breve), or dehydrated fermented milk. Intestinal barrier capacity to macromolecules was assessed in an Ussing chamber, and sensitization to cow's milk proteins was measured by systemic anti-beta-lactoglobulin immunoglobulin G1 titers and by intestinal anaphylaxis, the latter assessed by the beta-lactoglobulin-induced increase in short-circuit current of jejunal fragments (deltaIsc(beta-LG)). RESULTS: The electrical resistance of jejunum was similar in the four groups (approximately 80 omega/cm2) suggesting the same paracellular permeability. The transport of 14C-beta-lactoglobulin from mucosa to serosa was significantly decreased in the animals fed dehydrated fermented milk (403+/-131 ng / hr x cm2) compared with that in control animals or animals fed milk (767+/-250 ng / hr x cm2 and 749+/-475 ng / hr x cm2, respectively; p < 0.05). Milk fermentation did not modify native beta-lactoglobulin concentration but anti-beta-lactoglobulin immunoglobulin G1 titers were higher in fermented milk and dehydrated fermented milk (log10 titer = 2.86 and 2.79, respectively) than in guinea pigs fed milk (log10 titer = 2.5; p < 0.007). However, beta-lactoglobulin-induced intestinal anaphylaxis remained the same in the three groups (deltaIsc(beta-LG), 9.6+/-4.1 microA/cm2, 8.5+/-4.3 microA/cm2, and 8.5+/-3.4 microA/cm2 in milk-fed, fermented milk-fed, and dehydrated fermented milk-fed guinea pigs, respectively). CONCLUSIONS: The intestinal barrier capacity to milk proteins seems to be reinforced by dehydrated fermented milk, but milk and fermented milks are equally efficient in inducing cow's milk allergy in guinea pigs.

Animals↗
PubMed1998

The influence of apoptosis on intestinal barrier integrity in rats.

BACKGROUND: Apoptosis is a critical step responsible for maintaining the cellular balance between proliferation and death and for controlling tumorigenesis. Although an increase in intestinal apoptotic cells has been considered to be associated with the pathogenesis of gastrointestinal injury, little is understood concerning the role of apoptosis in the development of intestinal barrier dysfunction. METHODS: Apoptosis induced by intraperitoneal injection of doxorubicin in rats was evaluated by transmission electron microscopy and the TUNEL histochemistry method. Treatment with deoxy-D-glucose (a glycolytic pathway inhibitor) or cycloheximide (a protein synthesis inhibitor) was performed after doxorubicin challenge. Passage of human serum albumin from blood to the intestinal interstitium and the intestinal lumen or from the intestine to the intestinal interstitium and blood was evaluated by means of albumin clearance. RESULTS: A significant increase in gut water content, albumin flux, and bidirectional clearance of albumin accompanied by apoptotic epithelial cell increase was noted in doxorubicin-challenged rats treated with saline. The increase in endothelial and epithelial permeability and the increase of apoptosis could partly be prevented by treatment with deoxy-D-glucose or cycloheximide. CONCLUSION: Doxorubicin-increased epithelial apoptosis within the intestine occurs simultaneously with increased bidirectional permeability of the intestinal barrier, probably associated with both glycolytic and protein synthesis pathways. Apoptosis may thus play a role in the pathogenesis of intestinal barrier dysfunction.

Animals↗
PubMed2005

Modulation of intestinal barrier properties by miltefosine.

Miltefosine (hexadecylphosphocholine, HePC) is the first effective oral agent for the treatment of visceral leishmaniasis. This study aimed to determine whether this oral administration alters the integrity and transport capacities of the intestinal barrier. The objectives of this study were: (i) to evaluate the cytotoxicity of HePC, (ii) to investigate the effects of HePC on paracellular and transcellular transport and (iii) to investigate the influence of HePC on three major transporters of the intestinal barrier, namely, P-glycoprotein, the human intestinal peptide transporter (PepT-1) and the monocarboxylic acid transporter (MCT-1) in Caco-2 cell monolayers, used as an in vitro model of the human intestinal barrier. We show that HePC reduced the transepithelial electrical resistance and increased D-[14C]mannitol permeability in a dose-dependent manner but had no effect on [3H]testosterone permeability, demonstrating that HePC treatment enhances paracellular permeability via an opening of the tight junction complex without affecting the transcellular route. Morphological studies using confocal fluorescence microscopy showed no perturbation of the normal distribution of ZO-1, occludin or E-cadherin but revealed a redistribution of the tight junction-associated protein claudin-1 and the perijunctional actin after incubation with HePC. Finally, HePC was found to inhibit the intestinal P-glycoprotein in the Caco-2 cell model after a single short exposure. These results suggest that HePC could modify the oral bioavailability of other therapeutic compounds absorbed via the paracellular route or which are substrates of the intestinal P-glycoprotein.

Actin Cytoskeleton↗
PubMed2002

PKC-zeta is required in EGF protection of microtubules and intestinal barrier integrity against oxidant injury.

Using monolayers of human intestinal (Caco-2) cells, we showed that epidermal growth factor (EGF) protects intestinal barrier integrity against oxidant injury by protecting the microtubules and that protein kinase C (PKC) is required. Because atypical PKC-zeta isoform is abundant in wild-type (WT) Caco-2 cells, we hypothesized that PKC-zeta mediates, at least in part, EGF protection. Intestinal cells (Caco-2 or HT-29) were transfected to stably over- or underexpress PKC-zeta. These clones were preincubated with low or high doses of EGF or a PKC activator [1-oleoyl-2-acetyl-sn-glycerol (OAG)] before oxidant (0.5 mM H(2)O(2)). Relative to WT cells exposed to oxidant, only monolayers of transfected cells overexpressing PKC-zeta (2.9-fold) were protected against oxidant injury as indicated by increases in polymerized tubulin and decreases in monomeric tubulin, enhancement of architectural stability of the microtubule cytoskeleton, and increases in monolayer barrier integrity toward control levels (62% less leakiness). Overexpression-induced protection was OAG independent and even EGF independent, but EGF significantly potentiated PKC-zeta protection. Most overexpressed PKC-zeta (92%) resided in membrane and cytoskeletal fractions, indicating constitutive activation of PKC-zeta. Stably inhibiting PKC-zeta expression (95%) with antisense transfection substantially attenuated EGF protection as demonstrated by reduced tubulin assembly and increased microtubule disassembly, disruption of the microtubule cytoskeleton, and loss of monolayer barrier integrity. We conclude that 1) activation of PKC-zeta is necessary for EGF-induced protection, 2) PKC-zeta appears to be an endogenous stabilizer of the microtubule cytoskeleton and of intestinal barrier function against oxidative injury, and 3) we have identified a novel biological function (protection) among the atypical isoforms of PKC.

Caco-2 Cells↗
PubMed2000

Nitric oxide and its metabolites mediate ethanol-induced microtubule disruption and intestinal barrier dysfunction.

Loss of gastrointestinal (GI) barrier integrity has been implicated in a wide range of inflammatory illnesses, including alcoholic cirrhosis. Using monolayers of Caco-2 (intestinal) cells as a model, we showed that the ability of ethanol (EtOH) to disrupt intestinal barrier integrity depends on damage to the microtubule (MT) cytoskeleton, especially oxidative injury. One drug that prevented both the MT damage and barrier disruption was L-N(6)-1-iminoethyl-lysine, a selective inhibitor of the inducible form of nitric-oxide synthase (iNOS). Because of this finding and because overproduction of nitric oxide (NO) and generation of peroxynitrite (ONOO(-)) have been proposed to be responsible for mucosal injury in other GI disorders, we sought to determine whether NO overproduction and ONOO(-) formation mediates EtOH-induced MT damage and loss of intestinal barrier function. To this end, Caco-2 monolayers were exposed to EtOH or to authentic ONOO(-) or ONOO(-) generators with or without pretreatment with iNOS inhibitors or antioxidants. We found that EtOH caused 1) iNOS activation, 2) NO overproduction, 3) increases in oxidative stress and superoxide anion production (superoxide dismutase quenchable fluorescence of dichlorofluorescein), 4) nitration and oxidation of tubulin (immunoblotting), 5) decreased levels of stable polymerized tubulin, and 6) increased levels of disassembled tubulin. EtOH also 7) extensively damaged the MT cytoskeleton and 8) disrupted barrier function. Authentic ONOO(-) or ONOO(-) donors had similar effects. Pretreatment with a selective iNOS inhibitor, L-N(6)-1-iminoethyl-lysine, or with antioxidants (ONOO(-) scavengers urate or L-cysteine; superoxide anion scavenger superoxide dismutase) attenuated damage due to EtOH or to ONOO(-) generators. We conclude that EtOH-induced MT damage and intestinal barrier dysfunction require iNOS activation followed by NO overproduction and ONOO(-) formation. These findings provide a rationale for the development of novel therapeutic agents for alcohol-induced GI disorders that inhibit this mechanism.

Antioxidants↗
PubMed1998

Alterations in intestinal barrier function do not predispose to translocation of enteric bacteria in gastroenterologic patients.

Bacterial translocation from the intestinal lumen has been demonstrated in humans. Three mechanisms have been suggested to explain the phenomenon: altered intestinal barrier function, bacterial overgrowth, and impaired host defense. The aim of this study was to determine whether changes in intestinal barrier function assessed by measurement of intestinal permeability and morphology were associated with alteration in bacterial translocation. Intestinal permeability was assessed in 43 patients by the lactulose/L-rhamnose test with a 5-h urine collection. Mucosal atrophy was assessed from the villus height-to-mucosal thickness ratio in small-bowel biopsies. Bacterial translocation was determined by microbiologic analysis of harvested mesenteric lymph nodes. No significant differences were apparent in the incidence of bacterial translocation in patients with normal permeability (5 [23%] of 22 patients translocated) compared with patients with increased permeability (4 [19%] of 21 patients translocated). Similarly, no correlation was apparent between the incidence of bacterial translocation and the index of villus atrophy. The degree of villus atrophy failed to correlate with gastrointestinal permeability. These data suggest that the incidence of bacterial translocation is not related to increased intestinal permeability or mucosal atrophy.

Adult↗
PubMed1999

Butyrate from bacterial fermentation of germinated barley foodstuff preserves intestinal barrier function in experimental colitis in the rat model.

BACKGROUND AND AIMS: The consumption of germinated barley foodstuff (GBF) prevents inflammation and diarrhoea in a colitis model. In this study we investigated the mechanism of the preventative effect of GBF on experimental colitis in rats, in view of production of bacterial butyrate and preservation of intestinal barrier function. METHODS: Sprague-Dawley rats administered with diets supplemented with 3.5% dextran sodium sulphate were used as an experimental colitis model. Butyrate was given to rats orally or intracaecally. Intestinal barrier function was estimated by light microscopic observation of the mucosa, intestinal permeability and bacterial translocation. RESULTS: Mucosal damage was reduced by intracaecal administration of butyrate, but not by oral administration. Bacterial butyrate production and reduction of mucosal damage depended on the dose of GBF in diets. The action of endogenous bacterial butyrate, including the reduction of intestinal permeability and bacterial translocation, was inhibited by administration of an inhibitor of beta-oxidation of short-chain fatty acids. CONCLUSIONS: The feeding of GBF promotes bacterial butyrate production and improves intestinal barrier function in rats, resulting in mitigation of experimental colitis.

Animals↗