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PubMed1993

The level of immunoglobulins in the small and large intestinal mucosa from children with ulcerative colitis.

In 42 children 4 to 16 years old with ulcerative colitis by using peroxidase method and monoclonal antibodies we evaluated the presence of immunoglobulin A, M, G, E in the mucosa of the large and small intestines. It was found that the distribution of immunoglobulins in the acute phase was similar in the intestinal segments studied, which supports the opinion that the whole intestine has a common immune system playing a major role in the pathogenesis of the disease.

Adolescent↗

PubMed1991

Expression of HLA-DQ antigens in the small-intestinal mucosa of patients with coeliac disease.

Studies at the DNA and product level of B-cell lines of coeliac patients have shown a strong association between coeliac disease and the HLA-DQ alpha 2.3 and HLA-DQ beta 2.7 alleles. The monoclonal antisera SFR20-DQ alpha 5 and XIII-358.4, which specifically react with HLA-DQ alpha 2.3 and with HLA-DQ beta 2.3 and -DQ beta 2.7, respectively, have been used to detect the expression of these specificities in the small-intestinal mucosa of 7 coeliac patients and 11 non-coeliac persons. An immunoperoxidase technique on frozen tissue sections of jejunal biopsy specimens was used. Positive specimens showed immunoperoxidase staining of lymphocytes and histiocytes in the lamina propria. The epithelial cells showed no immunoperoxidase staining. Positive results at the intestinal level correlated with the HLA typing of the patients and controls. The distribution found for the HLA-DQ alleles in the intestinal mucosa makes the role of a HLA-DQ alpha/beta dimer as gliadin receptor at the epithelial cell less probable, but it is compatible with the hypothesis that these DQ molecules are involved in the regulation of the intestinal immune response to gluten.

Adult↗

PubMed1991

[Immunologic defects in the lymphatic system of the intestinal mucosa in common variable immunodeficiency (CVID) syndrome].

The humoral immune system of the intestinal mucosa of patients with common variable immuno deficiency (CVID) syndrome was studied immunohistologically using antibodies against immunoglobulin (Ig) A1-2, M and G1-4, against the J chain and the secretory component. In 9/13 CVID-patients IgA-positive cells were totally absent whereas a total IgM-defect was found only in 3/14 patients. Considerable numbers of J chain-positive cells were present in all CVID-patients irrespective of the extent of the Ig-defect indicating the presence of early B-cells unable to differentiate and to produce Ig. There was a strong expression of the secretory component in the cytoplasm and at the surface of enterocytes even in those CVID-patients who were totally defective in IgA- and IgM-positive cells.

Humans↗

PubMed1992

Helicobacter muridarum sp. nov., a microaerophilic helical bacterium with a novel ultrastructure isolated from the intestinal mucosa of rodents.

Helical organisms with novel ultrastructural characteristics were isolated from the intestinal mucosa of rats and mice. These bacteria were characterized by the presence of 9 to 11 periplasmic fibers which appeared as concentric helical ridges on the surface of each cell. The cells were motile with a rapid corkscrewlike motion and had bipolar tufts of 10 to 14 sheathed flagella. The bacteria were microaerophilic, nutritionally fastidious, and physiologically similar to Helicobacter species and Wolinella succinogenes but could be differentiated from these organisms by their unique cellular ultrastructure. Using 16S rRNA sequencing, we found that strain ST1T (T = type strain) was related to previously described Helicobacter species, "Flexispira rappini," and W. succinogenes. The closest relatives of strain ST1T were Helicobacter mustelae and "F. rappini" (average similarity value, 96%). On the basis of phylogenetic data, strain ST1T (= ATCC 49282T) represents a new species of the genus Helicobacter, for which we propose the name Helicobacter muridarum.

Animals↗

PubMed1976

[The effect of cytostatic therapy with vincristin sulphate on disaccarchidases of rat intestinal mucosa (author's transl)].

This report shows that appropriate doses of vincristin sulphate may decrease disaccharidase activities of intestinal mucosa. With the higher doses of the cytostatic drug, the drastic drop of enzyme activities is associated with morphological alterations of the mucosa; disacchardiase activities remain depressed at least for a couple of days even after full morphological restoration of the mucosa. Studies in man should reveal whether similar intestinal lesions occur due to therapeutic doses of vincristin sulphate.

Animals↗

PubMed1982

The action of six lipid perturbing substances on hormone receptor adenylate cyclase complex in turkey erythrocytes and intestinal mucosa cells.

Adenylate cyclase and beta-receptor binding in turkey erythrocytes is studied under the influence of dioctyl sodium sulphosuccinate (DSS), sodium dodecyl sulphate (SDS), sodium deoxycholate (DOC), filipin, oxyphenisatine and ethanol. Intact and lysed erythrocytes and erythrocyte membranes were investigated. In general the fluoride stimulated enzyme was most resistant to the action of the substances followed by the ligand binding, the hormone stimulated enzyme being most sensitive to the action of the substances. However, in certain ranges of concentrations, DSS, SDS, filipin and oxyphenisatine could further stimulate the fluoride stimulated enzyme. The adenylate cyclase in intestinal mucosa cells was studied in the presence of DSS, SDS, DOC and oxyphenisatine. The fluoride stimulated enzyme was here less stable than the basal enzyme activity, and two of the substances (SDS and oxyphenisatine) stimulating the erythrocyte enzyme could not stimulate the fluoride stimulated intestinal mucosa cell enzyme.

Adenylyl Cyclases↗

PubMed2006

Effect of noise on the morphology of the intestinal mucosa in laboratory rats.

To determine whether noise-induced stress disrupts the intestinal mucosa of laboratory rats, one group of 8 rats ("noise" rats) was subjected to 15 min of white noise (90 dB) daily for 3 wk. Another group ("quiet"rats) was housed for 3 wk in an acoustically similar room but with no additional noise. A 3rd group ("recovery" rats) was housed in the noise room for 3 wk and then in the quiet room for a further 3 wk. The ilea were fixed for microscopy. Villi adjacent to Peyer patches showed significantly more degranulated mast cells (mean+/-standard error of the mean, 3.95+/-0.80 versus 0.35+/-0.29, respectively) and eosinophils (mean+/-standard error of the mean, 9.46+/-0.44 versus 4.58+/-0.38) per villus section in noise rats than in quiet rats. Similar results were obtained with rooms reversed, to account for any differences in room characteristics. The mean width of villus laminar propria was significantly greater in noise rats than quiet rats, suggesting edema. In addition, mucosal epithelial cells of noise rats were often separated, sometimes detaching from the basement membrane, whereas those of quiet rats were intact. Behaviorally, noise rats exhibited significantly more grooming and rearing than quiet rats. Compared with noise rats, recovery rats showed no reduction in mast cell degranulation or mean width of villus lamina propria, but there were increased numbers of secreting goblet cells in villi adjacent to Peyer patches and some recovery of epithelial integrity.

Animal Welfare↗

PubMed1991

Regulation of ketone formation and phosphoenolpyruvate carboxykinase activity in the small intestinal mucosa of infant rats.

We studied the effect of different hormones added in vivo or in vitro on ketogenesis and phosphoenolpyruvate carboxykinase (PEPCK) activity in the small intestinal mucosa of suckling rats. Injection of insulin or dexamethasone in vivo or of an antiglucagon antiserum decreased the rate of ketone formation in the mucosa whereas injection of anti-insulin antiserum led to increased mucosal ketogenesis. PEPCK activity in the mucosa was decreased by the antiglucagon serum but was not affected by insulin or anti-insulin serum injections. Both liver and brown fat PEPCK responded as expected with the activity being elevated by anti-insulin serum and depressed by both insulin and antiglucagon serum. In the in vitro experiments, no effect of any of the agents on PEPCK was found. Ketone formation was suppressed in vitro by insulin or dexamethasone addition to the medium.

Animals↗

PubMed2001

IL-5 and TNF-alpha participate in recruitment of eosinophils to intestinal mucosa in ulcerative colitis.

There is an increased influx of activated eosinophils to the intestinal mucosa in active ulcerative colitis, and an increased release of eosinophil-derived proteins, such as ECP, has also been observed. These findings indicate that eosinophils may contribute to tissue damage and intestinal inflammation in this disease. The relative importance of different chemotactic factors and the impact of steroid treatment on their effect in active ulcerative colitis are not known. We measured the eosinophil chemotactic activity in perfusion fluids from 11 patients with ulcerative colitis before and after steroid treatment and from 7 control patients. The effect of neutralizing antibodies to IL-5 and -8, RANTES, eotaxin, MCP-3, TNF-alpha, GM-CSF was investigated. The chemotactic activity was higher in perfusion fluids from patients than from controls (P = 0.0043). Anti-IL-5 (P = 0.005) and -TNF-alpha (P = 0.017) inhibited the activity in perfusion fluids obtained before treatment. Steroid treatment prevented the effect of all antibodies but had no significant effect on the chemotactic activity. The chemotactic activity correlated with the levels of eosinophil granule proteins in the perfusion fluids. In conclusion, in ulcerative colitis, eosinophils are attracted to the intestinal tissue by chemotactic factors, of which IL-5 and TNF-alpha may be the most prominent steroid-sensitive ones. The steroid-insensitive chemotactic activities remain unidentified.

Adult↗

PubMed1975

Microvascular control in intestinal mucosa of normal and hemorrhaged rats.

The mucosal microcirculation in innervated and denervated small intestine was studied using anesthetized rats. Denervation did not cause significant (P greater than 0.05) diameter changes in the precapillary vasculature; however, venules did constrict significantly. These results indicate minimum neural control in the precapillary vasculature during the resting state. The innervated precapillary vasculature constricted during both the carotid occlusion reflex and hemorrhagic hypotension. The diameter of the denervated precapillary vasculature was unchanged during the carotid occlusion reflex and dilated during hemorrhage. The responses of innervated and denervated precapillary vasculatures were attributed to increased neural activity and autoregulatory mechanisms, respectively. Neither innervated nor denervated venules responded during the carotid occlusion reflex. During hemorrhage, however, innervated venules constricted and denervated vessels dilated. The vasoconstriction of the innervated vasculature during hemorrhage contributed to a stoppage of blood and epithelial detachment; these responses did not occur in the dilated, denervated vasculature. Therefore, neural vasoconstriction, qualitatively similar to that in normal animals during the baroreceptor reflex, is a contributing cause to the vascular and tissue impairment in the intestinal mucosa during hemorrhage.

Animals↗

PubMed1997

Vibrio mimicus attaches to the intestinal mucosa by outer membrane hemagglutinins specific to polypeptide moieties of glycoproteins.

Vibrio mimicus is the closest organism to Vibrio cholerae. V. mimicus E-33, which is a highly adhesive and enteropathogenic strain, is known to produce three types of hemagglutinins (HAs), i.e., a 31-kDa exocellular metalloprotease (Vm-HA/protease), lipopolysaccharide (Vm-LPSHA), and a 39-kDa major outer membrane protein (Vm-OMPHA). Hemagglutination induced by Vm-LPSHA and Vm-OMPHA was inhibited by glycoproteins, including mucin, fetuin, and asialofetuin, but not by monosaccharides, disaccharides, or N-acetylated saccharides. The inhibitory potential of each glycoprotein for Vm-OMPHA was greatly augmented by treatment with a glycolytic enzyme such as beta-D-galactosidase or beta-D-glucosidase, while pronase treatment achieved complete abolition of the inhibitory potential. The inhibitory ability of the glycoproteins for Vm-LPSHA was also abolished by pronase treatment; however, glycolytic enzyme treatment showed no effect. Hence, the polypeptide portion of glycoproteins may directly associate with Vm-OMPHA and Vm-LPSHA, but the sugar moiety may act as a barrier to interaction with Vm-OMPHA. The glycoproteins as well as Fab antibodies against Vm-OMPHA and Vm-LPSHA eliminated the ability of E-33 cells to agglutinate rabbit erythrocytes and to attach to rabbit intestinal mucosa. Additionally, expression of the hemagglutinating ability by the bacterial cells was accompanied by efficient bacterial adherence to the intestinal mucosa. Finally, the hemagglutinating activity of Vm-OMPHA was markedly increased by incubation with Vm-HA/protease. These results indicate that all three HAs may have significant roles in the glycoprotein-mediated intestinal adherence of V. mimicus E-33.

Animals↗

PubMed1982

[Activity of various enzymes of the intestinal mucosa in spontaneous colibacteriosis in pigs].

The aim of this work was to find out the histochemical activity of alkaline and acid phosphatases, and nonspecific esterases in intestinal mucosa in spontaneous swine colibacillosis. The investigated animals were divided into 3 groups: I--oedema disease (12 pigs), II--enetrotoxemia due to E. coli (8 pigs), III--control animals (5 pigs). The above grouping was based on the clinical, bacteriological and post-mortem examination. A slight increase of alkaline phosphatase activity in the jejunum and ileum of sick pigs was observed. The acid phosphatase activity decreased in the duodenum of oedema diseased pigs, while it increased in the cecum and colon--comparing with the control and enterotoxemia groups of animals. The decrease of acid phosphatase activity was observed in the jejunum and ileum of the enterotoxemia group of animals. The difference in the activity of nonspecific esterases concerned only the cecum and colon of diseased pigs, where its decrease was observed.

Acid Phosphatase↗

PubMed1985

A comparison of the effects of duodenal glucose infusion on carbohydrate and lipid metabolism in liver, adipose tissue and small intestinal mucosa in sheep.

The effects of duodenal glucose infusion on the specific activities of some enzymes of carbohydrate and lipid metabolism in the liver, perinephric adipose tissue and small intestinal mucosa of sheep were examined. Lipogenic enzyme activity was generally greatest in adipose tissue and lowest in liver and the response of these enzymes to glucose infusion was similarly greatest in adipose tissue. Glycolytic enzyme activity was significantly increased in all three tissues following duodenal glucose infusion. The effects of increasing carbohydrate availability in the small intestine in relation to tissue metabolism in sheep are discussed.

Adipose Tissue↗

PubMed2006

Effects of Saccharomyces boulardii on intestinal mucosa.

Saccharomyces boulardii (S. boulardii) is a non-pathogenic biotherapeutic agent, widely prescribed in a lyophilized form in many countries over the world. S. boulardii acts as a shuttle liberating effective enzymes, proteins and trophic factors during its intestinal transit that improve host immune defenses, digestion, and absorption of nutrients. In addition, S. boulardii secretes during its intestinal transit polyamines, mainly spermine and spermidine that regulate gene expression and protein synthesis. In this review, we will focus on the interactions of the yeast with the host intestinal mucosa.

Animals↗

PubMed2006

Gliadin-specific type 1 regulatory T cells from the intestinal mucosa of treated celiac patients inhibit pathogenic T cells.

Celiac disease (CD) results from a permanent intolerance to dietary gluten and is due to a massive T cell-mediated immune response to gliadin, the main component of gluten. In this disease, the regulation of immune responses to dietary gliadin is altered. Herein, we investigated whether IL-10 could modulate anti-gliadin immune responses and whether gliadin-specific type 1 regulatory T (Tr1) cells could be isolated from the intestinal mucosa of CD patients in remission. Short-term T cell lines were generated from jejunal biopsies, either freshly processed or cultured ex vivo with gliadin in the presence or absence of IL-10. Ex vivo stimulation of CD biopsies with gliadin in the presence of IL-10 resulted in suppression of Ag-specific proliferation and cytokine production, indicating that pathogenic T cells are susceptible to IL-10-mediated immune regulation. T cell clones generated from intestinal T cell lines were tested for gliadin specificity by cytokine production and proliferative responses. The majority of gliadin-specific T cell clones had a Th0 cytokine production profile with secretion of IL-2, IL-4, IFN-gamma, and IL-10 and proliferated in response to gliadin. Tr1 cell clones were also isolated. These Tr1 cells were anergic, restricted by DQ2 (a CD-associated HLA), and produced IL-10 and IFN-gamma, but little or no IL-2 or IL-4 upon activation with gliadin or polyclonal stimuli. Importantly, gliadin-specific Tr1 cell clones suppressed proliferation of pathogenic Th0 cells. In conclusion, dietary Ag-specific Tr1 cells are present in the human intestinal mucosa, and strategies to boost their numbers and/or function may offer new therapeutic opportunities to restore gut homeostasis.

Adolescent↗

PubMed2006

Dietary insulin affects leucine aminopeptidase, growth hormone, insulin-like growth factor I and insulin receptors in the intestinal mucosa of neonatal pigs.

BACKGROUND: Recent studies suggest that milk-borne insulin may regulate the development of the gastrointestinal tract in neonatal mammals. OBJECTIVES: To explore the mechanism by which milk-borne insulin affects gastrointestinal tract development, we examined the effect of dietary insulin on the expression levels of leucine aminopeptidase (LAP) and insulin-like growth factor I (IGF-I), as well as its effect on growth hormone (GH), IGF-I and insulin receptors in the small intestinal mucosa of neonatal pigs. METHODS: Five piglets were anesthetized and sampled within 2-4 h after birth. They were not allowed to suckle and were used as newborn controls (group N). Ten other piglets from 5 litters were randomly divided into group M (n=5), which was fed cow's milk, and group MI (n=5), which was fed cow's milk and insulin (2.5 mg/l). Piglets in groups M and MI were artificially fed for 3 days and then sampled. Total RNA in their intestinal mucosa was extracted with Tripure reagents (Roche, USA). Reverse transcription PCR (RT-PCR) was used to semi-quantify mRNA levels of target genes and 18S rRNA was used in an RT-PCR system as an internal control. PCR products were loaded onto a 9% nondenaturing polyacrylamide gel. The gel was stained by silver staining agents. Digital photos were taken and the strength of the band areas was quantified using software. RESULTS: The results showed that the DNA contents and LAP activity in the small intestines of the piglets in group MI were higher (p<0.05) than in the piglets in group N. Compared with group M, piglets in group MI exhibited significantly increased expression levels of both insulin and GH receptor in the ileum, and LAP in the jejunum (p<0.05); IGF-I receptor expression levels in both the jejunum and ileum were significantly decreased (p<0.01 and p<0.05, respectively), while IGF-I expression was unchanged (p>0.05). CONCLUSION: Collectively, dietary insulin increased mRNA levels of insulin and GH receptor, which could help explain the effect of dietary insulin on receptor-mediated postnatal development of the small intestine. Dietary insulin suppressed IGF-I receptor expression, which may be the result of negative feedback caused when insulin binds to IGF-I receptors.

Animal Feed↗

PubMed2002

[Dynamics of morphological changes in tissues from the pancreas, liver, and the small intestine mucosa in acute pancreatitis].

In acute cryogenic pancreatitis, apart from morphological changes in the affected organ there come to be seen destructive changes in tissues of the liver and small intestine that is evidenced by development in the liver of reactive hepatitis which is, strickly speaking, a result of a toxic effect of the pancreatic tissue necrotic products. In the small intestinal mucosa the above events are manifested by reactive enteritis, in which case both inflammatory-and-destructive and adaptive-and-regenerative processes are clearly seen.

Acute Disease↗

PubMed1985

The nature of the natural killer (NK) cell of human intestinal mucosa and mesenteric lymph node.

The relationship of the mononuclear cell (MNC) from human intestinal mucosa and mesenteric lymph node mediating anti-K-562 activity with that of peripheral blood has been assessed. Depletion of macrophages did not alter the measured cytotoxicity confirming that the effector cells were lymphocytes. Complement lysis of Leu 7 and Leu 11b coated cells reduced intestinal natural killer (NK) activity by a similar degree to that of peripheral blood but mesenteric lymph node NK activity was affected to a lesser extent. The response in NK activity of mucosal and nodal MNC to short incubation with lymphoblastoid interferon was similar to that for peripheral blood MNC. Twenty-four hours incubation of MNC with low concentrations of purified interleukin-2 (IL-2) consistently augmented intestinal and nodal NK activity but failed to augment that of peripheral blood MNC. No differences between the inhibitory effects of cAMP and prostaglandin E2 on NK activity from the three sites were seen. In addition, inhibition of cyclo-oxygenase activity with indomethacin had no effect on NK activity of intestinal and peripheral blood MNC while the lipoxygenase inhibitor, nordihydroguaiaretic acid, suppressed intestinal and peripheral blood NK activity similarly. In conclusion, anti-K-562 activity by intestinal MNC is mediated by NK cells with similar phenotypic and functional properties to those of peripheral blood. However, the increased sensitivity of mucosal NK cells to IL-2 suggests that higher proportions of NK cell precursors may be present in intestinal MNC populations.

Antioxidants↗