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Results for “Intestinal Mucosa”

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At least 307 records · Page 17Linked to original sources

PubMed1990

Effects of an inhibitor isolated from human small intestine on organ culture of intestinal mucosa.

Endogenous mitotic inhibitors have been implicated as controlling mechanisms of intestinal epithelium proliferation. We previously reported the purification of an inhibitor of intestinal epithelial cells in culture isolated from a villous extract of human jejunum. This article describes the biologic effects of this inhibitor on organ cultures of rabbit intestinal mucosa. Our results reveal that (1) this factor is not cytotoxic; (2) it inhibits intestinal epithelial cell proliferation in a dose-dependent and reversible manner; (3) it does not appear to be species-specific; (4) it is specific to the digestive tract, and more particularly to the small intestine.

Animals↗

PubMed2006

[Studies of the possible mechanisms for protective effects of recombinant human growth hormone on intestinal mucosa barrier in rat sepsis].

OBJECTIVE: To investigate the protective effects of recombinant human growth hormone (rhGH) on intestinal mucosal barrier in rat sepsis and explore its possible mechanisms. METHODS: E. coli was injected intraperitoneally to produce rats sepsis models. Forty-two female SD rats were randomly divided into the control group (group C), sepsis group (group S) and treatment group (group T). Group S and group T were further divided into 1 d and 3 d subgroups (T1d,T3d, Sld, S3d), respectively. The expression of IGF-1 mRNA in liver, expression of Bcl-2 protein in intestine, bacteria translocation, the levels of growth hormone(GH) and insulin-like growth factor-1 (IGF-1) in plasma, and the histological appearance of intestine were determined dynamically by means of RT-PCR, radioimmunoassay, immunohistochemical staining and other corresponding methods, respectively. RESULTS: (1) rhGH could significantly attenuate intestinal mucosal injuries and ameliorate bacteria translocation on sepsis rats. (2) The levels of Bcl-2 protein expression in intestine in group T (T1d:2441 +/- 117; T3d: 3628 +/- 235) were obviously higher than those of group S (S1d: 321 +/- 36; S3d: 1873 +/- 57) (P < 0.01). (3) The plasma levels of GH in group T (T1d: 1.28 +/- 0.24 microg/L; T3d: 2.14 +/- 0.48 microg/L) increased markedly than those of group S (S1d: 0.74 -/+ 0.12 microg/L; S3d: 0.60 +/- 0.18 microg/L) (P < 0.01). (4) The plasma levels of IGF-1 in group T (Tld: 168.94 +/- 65.67 microg/L; T3d: 201.56 +/- 64.98 microg/L) elevated significantly than those of group S (Sld: 116.72 +/- 13.96 microg/L; S3d:107.50 +/- 23.53 microg/L) (P < 0.05). (5) The levels of liver IGF-1 mRNA in group T (Tld: 0.98 +/- 0.20; T3d: 1.76 +/- 0.17) were significantly higher than those in group S (S1d: 0.38 +/- 0.09; S3d: 0.46 +/- 0.10) (P < 0.01). CONCLUSION: rhGH conferred protective efficacy in maintaining the integrity of intestinal mucosal barrier against sepsis in rat. The possible mechanisms might involve the rhGH-diminished apoptosis of intestinal mucosa cells and the rhGH-maintained intestinal mucosa barrier via the roles of GH and IGF-1.

Animals↗

PubMed1990

The effect of protein-energy malnutrition and refeeding on the adherence of Salmonella typhimurium to small intestinal mucosa and isolated enterocytes in rats.

The adherence of fimbriated (Fim+) and nonfimbriated (Fim-) strains of Salmonella typhimurium to both isolated intestinal epithelial cells and intact intestinal mucosa of healthy and malnourished rats was investigated. Fim+ strains bound in significantly higher numbers than did Fim- strains to enterocytes isolated either from healthy or malnourished rats. Adherence to intact intestinal mucosa in situ was demonstrable with both Fim+ and Fim- bacteria, but Fim+ strains were preferred because they showed approximately twofold higher numbers of adhered bacteria compared to Fim- strains. Additionally, bacterial adherence to intact mucosa in situ was consistently higher in well-fed controls than in malnourished rats. Ultrastructural studies revealed marked cell destruction and lysis in malnourished rats, whereas no histological change was detected in the mucosa of control animals. These results suggest that malnutrition may lead to altered intestinal cell surfaces, thus increasing their susceptibility to infection through mechanisms that are different from adherence.

Animals↗

PubMed1987

Dexamethasone-induced alterations in the glycosphingolipids of rat proximal small-intestinal mucosa.

Prior studies have demonstrated that glucocorticoids can influence the structure and function of several different organs, including the small intestine. However, to date, the effects of glucocorticoids on the glycosphingolipids of the rat small intestinal mucosa have not been examined. In the present experiments, male albino rats of the Sherman strain were subcutaneously administered dexamethasone (100 micrograms/100 g body wt. per day) or diluent for 4 days, and the ceramide, acidic and neutral glycosphingolipid compositions of the proximal small intestine of these animals were examined and compared. The results of these studies demonstrate that dexamethasone administration: (1) increased the content and relative percentage of hematoside (GM3) in this tissue; (2) increased the percentage of N-glycoylneuraminic acid of hematoside; (3) decreased the percentage of the long-chain base phytosphingosine of hematoside, glucosyl- and globotriaosylceramide; and (4) did not appear to influence significantly the concentration of the neutral glycosphingolipids or ceramide in this tissue. These data, therefore, indicate that dexamethasone administration induces alterations in the glycosphingolipids, particularly hematoside, of rat small-intestinal mucosa.

Animals↗

PubMed1984

Ultrastructure of the intestinal mucosa in pigs experimentally inoculated with an edema disease-producing strain of Escherichia coli (0139:K12:H1).

The intestinal tissues from 11 pigs orally inoculated with Escherichia coli (E. coli, 0139:K12:H1) were examined by transmission electron microscopy. The colonization of E. coli along the small intestinal mucosa was found in seven principals without any major changes in the enterocytes from day 2 to day 7 after inoculation when the experiment was terminated. Lesions of vessels of the intestinal mucosa could be detected as early as two days after inoculation and persisted until the experiment was terminated. Lesions consisted of endothelial swelling and vacuolation, subendothelial fibrin deposition, perivascular edema, microthrombus formation, endothelial proliferation, and necrosis of the tunica media. The possible pathogenesis of the disease is discussed.

Adhesiveness↗

PubMed1994

Histochemical and ultrastructural studies of mast cells in the intestinal mucosa and skin of the opossum Didelphis albiventris.

The mast cells located in the intestinal mucosa of a non-eutherian mammal were studied in comparison with those in the skin of the ear. In the intestinal mucosa, the mast cells exhibited a more variable shape, larger cytoplasmic granules and greater sensitivity to fixatives regarding their staining towards Toluidine Blue. Ultrastructurally, these granules were more heterogeneous but lacked the crystalline content found in granules of skin mast cells; lipid body-like organelles were found only in the mucosa-located mast cells. Histochemically, they differed from skin mast cells by the absence of periodic acid-Schiff (PAS)-positive granules. Unlike the mucosal mast cells of the rat, they fluoresced brilliant yellow after berberine treatment, which is evidence of the presence of heparin.

Animals↗

PubMed1987

The use of biochemical parameters for a qualitative and quantitative assessment of ischemic damage to the small-intestinal mucosa.

Lactate dehydrogenase has been measured in the small-intestinal mucosa in order to assess its value as a marker for the effects of ischemia and of reperfusion. The decrease in specific activity of the enzyme illustrates the deleterious effect of reperfusion on the quality of the remaining epithelial cells. However, this parameter fails to detect the loss of epithelial cells, which is the major event during ischemia as well as during reperfusion. In contrast, the expression of enzyme activity per g protein of the underlying intestinal muscle allowed us, in addition, to assess quantitatively the loss of epithelial cells, in good agreement with the histological data.

Animals↗

PubMed1996

Purification and properties of thioltransferase from monkey small intestinal mucosa: its role in protein-S-thiolation.

Modification of protein thiol by mixed disulfide formation with low molecular weight cellular thiols has been proposed as one of the post-translational modifications of amino acid side chains and is known to be catalyzed by thioltransferase. Intestinal mucosa is susceptible to oxidative injury and is likely to form protein mixed disulfide during oxidative stress. In the present study thioltransferase was purified from monkey small intestinal mucosa and its role in protein-s-thiolation was investigated. The purified enzyme was homogeneous, as judged by polyacrylamide gel electrophoresis under reducing conditions. The enzyme, with a molecular weight of 52 kDa, was a monomeric protein, which showed optimum activity at pH 8.0 with hydroxyethyl disulfide as substrate. The enzyme specifically cleaved the disulfide bond of the synthetic substrate, hydroxyethyl disulfide, in the presence of reduced glutathione (GSH) with the formation of oxidized glutathione (GSSG) as shown by high performance liquid chromatography. The enzyme also catalyzed protein thiolation of monkey intestinal mitochondria when incubated with glutathione disulfide. These studies have shown that thioltransferase purified from intestinal mucosa could catalyze dethiolation and thiolation.

Animals↗

PubMed1995

[Effect of EPA-rich fat emulsion on the permeability of the rat intestinal mucosa].

TR8030 (TR) which was EPA (omega-3 fatty acid)-rich fat emulsion and Intralipos (IL) which contained much omega-6 fatty acids were administered intraperitoneally to rats to evaluate their effects on the intestinal mucosa by determining changes in the fatty acid composition of mucosal phospholipid, intra- and intercellular intestinal mucosal permeability, and thickness of the unstirred water layer, one of the intestinal defense functions. The content of EPA in the intestinal mucosa was higher in the TR group than in the control group, and there was a change in intercellular permeability. The unstirred water layer was thinner in the TR group than in the IL group. Based on the results presented, it may be concluded that EPA-rich emulsion affects the fatty acid composition of intestinal mucosa phospholipid, mucosal intercellular permeability, and mucosal defense function.

Animals↗

PubMed2006

Quantitative study of soybean-induced changes in proliferation and programmed cell death in the intestinal mucosa of young rats.

The use of soybean in human and animal nutrition is limited because of high content of bioactive compounds: enzyme inhibitors, polyphenols, goitrogens, phytates, saponins, sugars, and agglutinins. The damage of intestinal mucosa structure was previously observed in animals fed soybean supplemented diets. Hence, the objectives of the presented study were to compare intensity of epithelium remodeling processes in different intestinal segments, and to evaluate the influence of the 1% of soybean dietary supplementation on the processes in intestinal mucosa. The experiment was performed on 30 Wistar rats fed AIN-93 based diets. Animals were divided randomly into three groups: control (CTRL), with 1% of raw soybean (RS) and with 1% of soaked and boiled soybean (BS). The samples of: duodenum (DUO), proximal jejunum (PROX), mid-jejunum (MID), distal-jejunum (DIST) and ileum (ILE) were collected. The following processes in these samples were evaluated: mitosis (Ki-67), apoptosis (Cpp32), autophagy (MAP I LC3) and DNA damage (p53). Present data show that modification of soybean by soaking and subsequent boiling markedly influences the enterocyte turnover in the small intestine mucosa. Increased mitotic ratio in the intestine of rats fed with boiled soybean masks the negative effects of soybean on the small intestine structure.

Animals↗

PubMed1994

Short-term starvation alters the free amino acid content of the human intestinal mucosa.

1. The effects of short-term starvation and refeeding on the free amino acid concentrations of the intestinal mucosa were characterized in male subjects (n = 6), using endoscopically obtained biopsy specimens from the duodenum and from all four segments of the colon. 2. The alterations in the amino acid concentrations in response to short-term starvation were overall uniform in both duodenal and colonic mucosa as well as in plasma. Most amino acids decreased, whereas branched-chain amino acids increased. 3. In the colon, glutamic acid and glutamine decreased during the starvation period, whereas they remained unaltered in the duodenum. This was the major difference in response to short-term starvation between the amino acid concentrations in the intestinal mucosa of the duodenum and colon. 4. Refeeding for 3 days normalized the amino acid concentrations except for glutamic acid, asparagine and histidine, which remained low in the colon, and threonine, which showed an overshoot in both parts of the intestine. 5. The changes in mucosal amino acid concentrations seen in response to starvation and refeeding were uniform in the four segments of the colon. This suggests that sampling from the rectum/sigmoid colon will give representative values for the free amino acid concentrations of the entire large intestine.

Adult↗

PubMed1981

T lymphocyte subsets in human intestinal mucosa: the distribution and relationship to MHC-derived antigens.

T lymphocytes in the normal human intestinal tract have been analysed in tissue sections by a double-marker immunofluorescence technique, combining antiserum to T lymphocyte antigen (HuTLA) with a monoclonal antibody detecting T cells of suppressor-cytotoxic phenotype (OKT8). The distribution of HLA-A -B, -C and Ia-like antigens in intestinal mucosa was also examined by a similar method. In small and large intestine 67 to 90% (mean 70%) of intraepithelial T lymphocytes were of suppressor-cytotoxic phenotype (OKT8+). In contrast, only 27 to 56% (mean 39%) of lamina propria T cells were OKT8+. Intestinal epithelial cells demonstrated strong membrane staining for HLA-A, -B, -C antigens. Ia-like antigens were detected on the epithelial cells of small intestinal villi, but not on colonic epithelial cells. Lamina propria macrophages expressed both HLA-A, -B, -C and Ia-like antigens, the latter having strong membrane and cytoplasmic fluorescence. The distribution of T cells with suppressor-cytotoxic or inducer phenotype in the intestinal epithelium and lamina propria may be related to the differential expression of Ia-like and HLA-A, -B, -C antigens in intestinal mucosa.

Antibodies, Monoclonal↗

PubMed1995

Quantitative analysis and immunohistochemical studies on small intestinal mucosa of food-sensitive enteropathy.

Quantitative analysis and immunohistochemical studies of small intestinal mucosa were performed to investigate the mechanism of mucosal damage in 10 patients with food-sensitive enteropathy. Jejunal biopsy specimens were taken before and after treatment and after clinical relapse following a challenge test. The low villous height of untreated patients normalized after introduction of an elimination diet but declined again to subnormal level after a challenge test. Several other types of cells were significantly increased in the untreated patients in comparison to controls. These included HLA-DR+ (DR+) CD4+ cells in the lamina propria and intraepithelial CD8+ cells. Moreover, those cell patterns, such as increased DR+ CD4+ cells and CD8+ cells, normalized with treatment but regressed to pretreatment levels when the patients were challenged. These findings suggest that activated CD4+ cells in the lamina propria of the small intestinal mucosa, probably by releasing cytokines, may play an important role in contributing to mucosal damage in patients with food-sensitive enteropathy.

Animals↗

PubMed2003

Ca2+ signaling in identified T-lymphocytes from human intestinal mucosa. Relation to hyporeactivity, proliferation, and inflammatory bowel disease.

Ca2+ entry across the plasma membrane is necessary for the activation and proliferation of T-lymphocytes. Human intestinal lamina propria lymphocytes physiologically exhibit minimal proliferation in response to antigen receptor stimulation when compared with peripheral blood T-lymphocytes. This hyporeactivity is partially abolished in inflammatory bowel disease. We hypothesized that differences in Ca2+ signaling could be related to the disease. To test this possibility, we measured Ca2+ signals in identified lymphocytes from human blood and human intestinal mucosa. Ca2+ signals in lamina propria T-lymphocytes from non-inflamed tissue were drastically reduced when compared with Ca2+ signals of blood T-lymphocytes from the same persons. However, Ca2+ signals in T-lymphocytes from inflamed intestinal mucosa were much higher than the ones from non-inflamed mucosa and almost reached levels of Ca2+ signals in peripheral blood T-cells. Furthermore, Ca2+ influx was closely linked to cell proliferation in both peripheral blood T-lymphocytes and lamina propria lymphocytes cells. We conclude that differences in Ca2+ signaling can explain the differences of T-lymphocyte reactivity in blood versus lamina propria and, importantly, also between T-lymphocytes from inflamed and non-inflamed intestinal mucosa. Ca2+ channels in the plasma membrane of T-lymphocytes might thus prove an excellent target to screen for immunosuppressiva to potentially treat the symptoms of inflammatory bowel disease.

Calcium↗

PubMed1976

Isolation and characterization of iron-binding proteins from rat intestinal mucosa.

Two iron-binding proteins were isolated from rat intestinal mucosa. From determination of their molecular weights, their electrophoretic and iron-binding properties it was established that one was a mucosal ferritin and the other a mucosal transferrin. The mucosal ferritin is compared in its molecular weight, isoelectric point, amino acid composition and tryptic peptide pattern with the ferritins of rat spleen and liver. All three ferritins are distinctly different from one another. In addition the iron content of mucosal ferritin was found to be much lower than that of liver and spleen ferritins. Mucosal transferrin was separated into two components by isoelectric focusing, as was plasma transferrin. The plasma and mucosal transferrins differ in their isoelectric points and in their amino acid compositions. Differences were also found in vitro in the iron-binding of mucosal transferrin as compared with plasma transferrin. The role of these mucosal proteins in the absorption of iron is briefly discussed.

Amino Acids↗

PubMed1977

Association of some enterobacteria with the intestinal mucosa of mouse in relation to their partition in aqueous polymer two-phase systems.

The association of enterobacteria with mouse intestinal mucosa has been investigated by pumping heat-killed, radioactively-labelled bacteria through the gut lumen in vitro. Approximately 20 cm of the small intestine proximal to the ileo-caecal valve was rinsed, excised and maintained in an organ bath. By using two different bacteria labelled with different radioactive isotopes, the relative association of the two bacterial pumped through the same piece of gut was determined. Cross-labelling showed that choice of isotope did not affect the association. Salmonella typhimurium 395 MR10 was used as reference and the other bacteria investigated related to it. S. typhimurium MR10 and Escherichia coli O 14 K7, which are relatively lipophilic, showed greater association than S. typhimurium 395 MS and E. coli O 111 K58, which are more hydrophilic. Prolonged incubation of bacteria with the length of intestine in vitro leading to damage of the brush border of the mucosal epithelium enhanced the association of the bacteria. These data suggest that similar physico-chemical surface properies govern the association certain enterobacteria to the intestinal mucosa as in phagocytosis with professional phagocytes.

Acetylglucosaminidase↗

PubMed1970

Scanning and transmission electron microscopic studies of human intestinal mucosa.

The scanning electron microscope is capable of 25 mmu resolution combined with a great depth of focus, features which make the technique of value in the study of the intestinal mucosa. Surgical biopsies and postmortem specimens of small intestine have been examined using scanning and transmission electron microscopy. In biopsies, at low magnification, the villous pattern is seen while at higher magnification details of cell surfaces may be observed. Some features are best observed using scanning microscopy to examine dewaxed thick histological sections. In necropsy specimens villous architecture can still be satisfactorily assessed and details of the villous cores are seen, their collagen skeletons apparently less robust than the villi of the fresh biopsy. Scanning microscopy can extend the three-dimensional study of the small intestinal mucosa beyond the limits imposed by the resolution of the dissecting microscope.

Autolysis↗

PubMed1976

Isolation and characterization of four peptide hydrolases from the brush border of rat intestinal mucosa.

Peptide hydrolases (EC 3.4.-.-) were solubilized from purified brush borders of rat intestinal mucosa by papain digestion. Three peptide hydrolases, I, II, and III, with different substrate specificities were isolated by means of DEAE-cellulose chromatography and preparative acrylamide gel electrophoresis. On repeat preparative acrylamide gel electrophoresis under slightly different conditions, enzyme II was resolved into two proteins, IIa and IIb, with vary similar, possibly identical, substrate specificities. Efforts to discover additional brush border peptide hydrolases revealed none. Studies using more than 50 substrates showed that enzyme I was most active against Met-Met, Met-Ala, and Met-Phe while enzyme II was most active against Phe-Gly, Phe-Ser, and Leu-Gly-Gly, and enzyme III most rapidly hydrolyzed Gly-Leu, Leu-Gly, and Met-Gly. Efforts to discover substrates which are highly discriminating for each enzyme were partly successful. Thus, a number of substrates including leucine amide, leucyl-beta-naphthylamide and Phe-Asp were hydrolyzed almost exclusively (95% or more) by enzyme II while Gly-Leu was similarly specific for enzyme III. No substrate highly discriminating for enzyme I was discovered. Ion-exchange chromatography resulted in increases in specific activity of 10- and 120-fold for enzymes II and III, respectively. By sequential use of ion-exchange chromatography and preparative acrylamide gel electrophoresis, each of the three enzymes was partially purified to the point that they were free of contaminating disaccharidases and enzymes I and II gave single dense bands on analytical acrylamide gel electrophoresis while enzyme III gave a single dense band plus one additional faint protein band. Under appropriate conditions, analytical gel electrophoresis also resolved enzyme II into two bands with enzyme activity. The three enzymes were isolated from intestinal brush borders of germ-free rats indicating that none of the enzymes is of bacterial origin. With Phe-Gly as substrate, pH optima for enzymes I, II, and III were 8.0, 8.0, and 8.5, respectively. Molecular weights determined by gel filtration were 283 000, 284 000, and 134 000, respectively. Studies of activation by metal ions and inhibition by metal ion chelators suggested that the activity of each of the enzymes is dependent on a relatively tightly bound metal cofactor. Peptide hydrolases of the intestinal mucosa play an essential role in protein digestion. The studies presented here help to clarify the total number and substrate specificities of these enzymes in the rat brush border.

Animals↗