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At least 325 records · Page 18Linked to original sources
PubMed1990

Temperature adaptation of biological membranes: differential homoeoviscous responses in brush-border and basolateral membranes of carp intestinal mucosa.

The effects of temperature acclimation of carp upon the hydrocarbon order of intestinal membranes has been determined. A fractionation technique has been developed for the simultaneous purification of brush-border and basolateral membrane fractions from the intestinal mucosa. The specific activity of alkaline phosphatase in the brush-border fraction was enhanced 6.4-fold over that of the initial homogenate, whilst the (Na(+)-K+)-stimulated ATPase was enhanced 5.8-fold in the basolateral fraction. The specific activities of NADPH-cytochrome-c reductase, succinate-cytochrome-c reductase and acid phosphatase were not increased in these two fractions. Membrane hydrocarbon order in membranes from 10 and 30 degrees C-acclimated carp has been compared by measuring the steady-state fluorescence polarization of 1,6-diphenyl-1,3,5-hexatriene over a range of temperatures. In the brush-border fraction, polarization was identical in both cold- and warm-acclimated groups, whilst large differences were observed in the basolateral fraction sufficient to offset approx. 75% of the temperature-induced ordering effects of cold. The fatty acid composition of the major phosphoglyceride fractions in the brush-border fraction was also largely unaffected by thermal acclimation, whilst the basolateral fraction showed significant increases in the proportion of unsaturated fatty acids in the cold. It is concluded that whilst the basolateral membrane of intestinal mucosa displays a large homoeoviscous response that correlates with a shift in lipid composition, the brush-border membrane does not. These findings are consistent with evidence of functional adaptations of the basolateral membrane during thermal acclimation (Gibson, J.S., Ellory, J.C. and Cossins, A.R. (1985) J. Exp. Biol. 114, 355-364).

Adaptation, Physiological↗
PubMed1984

Characterization of somatostatin binding sites in cytosolic fraction of rat intestinal mucosa.

Specific binding sites for somatostatin have been characterized in cytosolic fraction of rat intestinal mucosa by using 125I-labelled Tyr11-somatostatin and a variety of physicochemical conditions. The binding depended on time, temperature and pH, and was reversible, saturable and specific. At apparent equilibrium, the specific binding of 125I-Tyr11-somatostatin was competitively inhibited by native somatostatin in the 1 nM-4 microM concentration range. Binding studies suggested the presence of two classes of binding sites: a class with high affinity (Kd = 0.07 microM) and low capacity (4.6 pmol/mg protein) and a class with low affinity (Kd = 1.05 microM) and high capacity (277 pmol/mg protein) at 25 degrees C. Somatostatin exhibited competitive inhibition of tracer binding, while neuropeptides such as neurotensin, substance P, Leu-enkephalin, and vasoactive intestinal peptide were ineffective. The presence of somatostatin binding sites in cytosolic fraction of intestinal mucosa, together with the known occurrence of somatostatin in D-cells and nerve endings in the small intestine, strongly suggest that this peptide may be involved in the physiology and physiopathology of intestinal epithelium.

Animals↗
PubMed1999

Morphological and immunohistochemical changes in intestinal mucosa and PYY release following total colectomy with ileal pouch-anal anastomosis in dogs.

Other studies have shown that both morphological and functional adaptation occur in the ileal mucosa after total colectomy and may be mediated by humoral factors. To elucidate the participation of peptide YY (PYY) in intestinal adaptation after total proctocolectomy with ileal pouch-anal anastomosis (IPAA), changes in the number of PYY-containing cells and in histological appearance in the intestinal mucosa, especially in the mucosa of ileal pouch, were investigated in dogs. We further examined changes in postprandial PYY release in relation to those in PYY-containing cells. Ten adult beagle dogs underwent IPAA. Before and 2, 6, and 12 months after surgery, a test meal was given, and blood samples were taken from a foreleg vein at intervals for 3 hr for measurements of plasma PYY concentration by radioimmunoassay. Before and one year after surgery, morphological studies of the intestinal mucosa were performed using parameters such as villous height (VH), mucosal thickness (MT), and villous index (VI). Immunohistochemical studies of PYY were also done in the intestinal mucosa. Both fasting and postprandial plasma PYY levels were reduced to half of the preoperative levels at two months after surgery. Thereafter, postprandial levels approached preoperative concentrations, while fasting levels remained unchanged. VH, MT, and VI were significantly smaller in the ileal pouch than in the ileal end of the controls. The MT of the ileal pouch was similar to that of the colon. PYY-containing cells in the mucosa of the ileal pouch were distributed more densely than those in the ileal end, similar to those in the colon of the controls. It was concluded that after IPAA, the pouch mucosa gradually changed to resemble the colonic mucosa not only in histological appearance but also in the population of PYY-containing cells. It is therefore considered that colonic transformation of the ileal-pouch mucosa is closely related to the increase in the number of PYY-containing cells and the steady recovery of postprandial PYY secretion.

Animals↗
PubMed1987

Identification and characterization of insulin receptors in basolateral membranes of dog intestinal mucosa.

Little is known about hormonal regulation of substrate transport and metabolism in the mucosal lining of the small intestine. Because insulin regulates these functions in other tissues by binding to its receptor, we have investigated the presence of insulin receptors in canine small intestinal mucosa with basolateral membranes (BLM) and brush border membranes (BBM) prepared by sorbitol density centrifugation. A14-[125I]iodoinsulin was used to study binding and structural characteristics of specific insulin receptors in BLM. Analysis of receptors in BLM identified binding sites with high affinity (Kd 88 pM) and low capacity (0.4 pmol/mg protein) as well as with low affinity (Kd 36 nM) and high capacity (4.7 pmol/mg protein). Binding was time, temperature, and pH dependent, and 125I-labeled insulin dissociation was enhanced in the presence of unlabeled insulin. Cross-reactivity of these receptors to proinsulin, IGF-II, and IGF-I was 4, 1.8, and less than 1%, respectively. Covalent cross-linking of labeled insulin to BLM insulin receptors with disuccinimidyl suberate revealed a single 135,000-Mr band that was completely inhibited by unlabeled insulin. There was a 16-fold greater specific binding of insulin to BLM (39.0 +/- 2.4%) than to BBM (2.5 +/- 0.6%). These results demonstrate the presence of a highly specific receptor for insulin on the vascular, but not the luminal, surface of the small intestinal mucosa in dogs, and suggest that insulin may play an important role in the regulation of gastrointestinal physiology.

Animals↗
PubMed1994

Gastric fundic inhibition of sugar transport across the intestinal mucosa of guinea-pig.

A low molecular weight peptide designated gastric fundic factor (GFF), extracted from porcine fundic mucosa and administered to the serosal surface of mucosal sheets from guinea-pig intestine, decreased the transport of luminal glucose across the sheets by up to 70%. The results show that gastric fundic inhibition of glucose absorption observed in different animal models in vivo can be reproduced in vitro, and suggest that the intestinal mucosa itself is the target for peptide hormone(s) released by the gastric fundic mucosa. Simultaneous transport of alpha-aminoisobutyric acid, a nonmetabolisable amino acid, through the jejunal mucosa was unaffected as was paracellular permeation by inulin. However, amino acid transport was also reduced when GFF was administered to sheets of ileal mucosa. The intestinal mucosal sheet in vitro is a sensitive and convenient model with which to follow the purification of GFF to homogeneity.

Aminoisobutyric Acids↗
PubMed1996

Selective increase of V beta 2+ T cells in the small intestinal mucosa in Kawasaki disease.

The current study tested the hypothesis that the gastrointestinal tract could be one of the primary sites of entry for etiologic agents in Kawasaki disease (KD). In an attempt to elucidate the pathogenic role of certain superantigenic agents in KD, T cell receptor V beta expression by T cells in the small intestinal mucosa of KD patients was investigated using MAb on frozen tissue sections. Twelve Japanese patients with KD and eight controls were enrolled in the study. The numbers of cells stained by an immunofluorescence from each study group were counted and analyzed statistically by the t test. The occurrence of V beta 2+ T cells was found to be selectively increased in the small intestinal mucosa of patients in the acute phase of KD compared with controls (p < 0.01). In our previous study, five kinds of streptococci and two kinds of staphylococci, not detected in control patients, were isolated from the lumen of the jejunum of KD patients. These data suggest that the increased occurrence of V beta 2+ T cells in the jejunal mucosa of KD patients may be caused by exotoxins acting as superantigens produced by bacteria colonizing the small intestinal mucosa of these patients.

Child, Preschool↗
PubMed1996

Evidence against T-cell development in the adult human intestinal mucosa based upon lack of terminal deoxynucleotidyltransferase expression.

Several lines of evidence indicate that a subset of murine intestinal intraepithelial lymphocytes (iIEL), particularly those which express the CD8 alpha alpha homodimer, mature extrathymically. This study confirms that a small fraction of adult human iIEL also express the CD8 alpha alpha homodimer and demonstrates that most of these cells in the small intestine are T cells using the alpha beta T-cell receptor (TCR). Whether these cells or other subsets of adult human iIEL mature extrathymically in the intestine was assessed by measuring the expression of terminal deoxynucleotidyltransferase (TdT), an enzyme expressed exclusively by immature lymphocytes. Very low levels of TdT message could be detected by polymerase chain reaction (PCR) amplification in some iIEL samples. The level of TdT expression was assayed by competitive PCR amplification and compared with thymocytes and peripheral blood lymphocytes. These measurements indicated that the number of immature T cells expressing TdT in the intestinal epithelium was less than one cell per 10(7) lymphocytes. This demonstrates that there are few if any TdT expressing immature T cells in the adult human intestinal mucosa and indicates, therefore, that T-cell development in the intestinal mucosa does not contribute significantly to the T-cell repertoire of the adult human intestine.

Adult↗
PubMed2003

Chronic allergy to dietary ovalbumin induces lymphocyte migration to rat small intestinal mucosa that is inhibited by MAdCAM-1.

Few models have described a chronic food allergy with morphological changes in the intestinal mucosa. Here we established an ovalbumin (OVA)-induced, cell-mediated, allergic rat model and examined lymphocyte migration in the gut. Brown Norway rats were intraperitoneally sensitized to OVA and then given 10 mg OVA/day by gastric intubation for 6 wk. Lymphocyte subsets and adhesion molecules were examined immunohistochemically, and the migration of T lymphocytes to microvessels of Peyer's patches and villus mucosa was observed by using an intravital microscope. Serum OVA-specific IgG and IgE levels were increased in animals repeatedly exposed to OVA. Significant villus atrophy and increased crypt depth was accompanied by increased infiltration of T lymphocytes in the small intestinal mucosa of the group given OVA. Expression of rat mast cell protease II and of mucosal addressin cell adhesion molecule-1 (MAdCAM-1) was also increased in these groups. The administration of anti-MAdCAM-1 antibody significantly attenuated the OVA-induced changes in the mucosal architecture and in CD4 T lymphocyte infiltration. Intravital observation demonstrated that in rats with a chronic allergy, T lymphocytes significantly accumulated in villus microvessels as well as in Peyer's patches via a MAdCAM-1-dependent process. Our model of chronic food allergy revealed that lymphocyte migration was increased with MAdCAM-1 upregulation.

Animals↗
PubMed2003

Alterations of intestinal mucosa structure and barrier function following traumatic brain injury in rats.

AIM: Gastrointestinal dysfunction is a common complication in patients with traumatic brain injury (TBI). However, the effect of traumatic brain injury on intestinal mucosa has not been studied previously. The aim of the current study was to explore the alterations of intestinal mucosa morphology and barrier function, and to determine how rapidly the impairment of gut barrier function occurs and how long it persists following traumatic brain injury. METHODS: Male Wistar rats were randomly divided into six groups (6 rats each group) including controls without brain injury and traumatic brain injury groups at hours 3, 12, 24, and 72, and on day 7. The intestinal mucosa structure was detected by histopathological examination and electron microscopy. Gut barrier dysfunction was evaluated by detecting serum endotoxin and intestinal permeability. The level of serum endotoxin and intestinal permeability was measured by using chromogenic limulus amebocyte lysate and lactulose/mannitol (L/M) ratio, respectively. RESULTS: After traumatic brain injury, the histopathological alterations of gut mucosa occurred rapidly as early as 3 hours and progressed to a serious state, including shedding of epithelial cells, fracture of villi, focal ulcer, fusion of adjacent villi, dilation of central chyle duct, mucosal atrophy, and vascular dilation, congestion and edema in the villous interstitium and lamina propria. Apoptosis of epithelial cells, fracture and sparseness of microvilli, loss of tight junction between enterocytes, damage of mitochondria and endoplasm, were found by electron microscopy. The villous height, crypt depth and surface area in jejunum decreased progressively with the time of brain injury. As compared with that of control group (183.7 +/- 41.8 EU/L), serum endotoxin level was significantly increased at 3, 12, and 24 hours following TBI (434.8 +/- 54.9 EU/L, 324.2 +/- 61.7 EU/L and 303.3 +/- 60.2 EU/L, respectively), and peaked at 72 hours (560.5 +/- 76.2 EU/L), then declined on day 7 (306.7 +/- 62.4 EU/L, P<0.01). Two peaks of serum endotoxin level were found at hours 3 and 72 following TBI. L/M ratio was also significantly higher in TBI groups than that in control group (control, 0.0172 +/- 0.0009; 12 h, 0.0303 +/- 0.0013; 24 h, 0.0354 +/- 0.0025; 72 h, 0.0736 +/- 0.0105; 7 d, 0.0588 +/- 0.0083; P<0.01). CONCLUSION: Traumatic brain injury can induce significant damages of gut structure and impairment of barrier function which occur rapidly as early as 3 hours following brain injury and lasts for more than 7 days with marked mucosal atrophy.

Animals↗
PubMed1984

Cavitation of mesenteric lymph nodes, splenic atrophy, and a flat small intestinal mucosa. Report of six cases.

This study describes, in 6 patients with a flat small intestinal mucosa and splenic atrophy, a particular lesion of the mesenteric lymph nodes termed "cavitation." In 4 women and 2 men with abdominal mass, intestinal obstruction, or suspected celiac disease-associated lymphoma, unusual pseudocystic lymph node lesions were found in the jejunal or jejunoileal mesentery. These lesions consisted histologically of a large central cavity occupied by hyaline-type material and surrounded by fibrous tissue and remnants of lymph node structures. There was no histologic evidence of malignant lymphoma or mesenteric panniculitis. Diffuse subtotal villous atrophy involving at least the jejunum was found in each case, together with unequivocal biological and morphological evidence of splenic atrophy, severe malabsorption, and a history of chronic or childhood diarrhea. HLA B8 or DR3, or both, was present in 4 of 4 cases; dermatitis herpetiformis was present in 1 case. An unequivocal mucosal response to a gluten-free diet was observed in 2 cases. Four patients died of cachexia or hyposplenism-related infections. We conclude that cavitation of mesenteric lymph nodes is an original feature which may be associated with splenic atrophy and a flat small intestinal mucosa; some of these patients may have celiac disease. Pathogenesis is unknown.

Adult↗
PubMed1999

Vitamin A prevents the decline in immunoglobulin A and Th2 cytokine levels in small intestinal mucosa of protein-malnourished mice.

We examined whether vitamin A improved mucosal immune depression in mice with wasting protein deficiency. In male C3H/HeN mice fed a semi-purified 1% protein diet for 2 wk, plasma retinol and immunoglobulin A (IgA) concentrations in the small intestinal mucosa were 50 and 55%, respectively, of those in mice fed a semi-purified 20% protein diet, (P < 0.05). Daily supplementation of 0.3 mg of retinyl acetate to protein-deficient mice for 2 wk increased the plasma retinol level to the value in the protein-sufficient mice. However, 1 mg/d of retinyl acetate was required to prevent the decline of the IgA level caused by the protein deficiency. Mice fed the low-protein diet had lower concentrations of IL-4 and IL-5 in the small intestinal mucosa and fewer IL-4- and IL-5-containing cells in the lamina propria (P < 0. 05). Retinyl acetate (1 mg) significantly restored the IL-5 level and the number of IL-4- and IL-5-containing cells. After immunization with 20 microg of cholera toxin (CT), the intestinal mucosa of protein-deficient mice contained significantly less CT-specific IgA than control mice. Treatment with 1 mg of retinyl acetate prevented the decline of anti-CT IgA level in the protein-deficient mice, improving their survival rate after an exposure to 0.1 mg of CT. These results suggest that large oral supplements of vitamin A may preserve mucosal IgA level during protein malnutrition, possibly by stimulating Th2 cytokine production and thereby, inducing resistance against infection.

Animals↗
PubMed1980

Purification of an enzyme with lysophospholipase activity from rat intestinal mucosa by hydrophobic chromatography.

A method based on hydrophobic chromatography is described for the purification of a lysophospholipase from the mucosa of rat small intestine. Under the conditions used, one single chromatographic run on phenyl-Sepharose CL-4B yielded a 582-fold purification with a 79% overall recovery of enzyme activity. A subsodium dodecyl sulphate gel electrophoresis; its isoelectric point is 5.6.

Animals↗
PubMed1980

[Autoradiographic investigations of age-dependent proliferation kinetics in the small intestine mucosa of rate (author's transl)].

Aging of cells depends on mitotic activity which is particularly evident in multicellular organisms. By means of histoautoradiography we studied the cell kinetics of the mucosa of the small intestine in a total of 244 Wistar rats aged 6 days, 6 weeks, 6, 12, 23 and 28 months, resp. We could demonstrate that the regeneration rate of cells per hour in the crypts of the small intestine and the migration velocity of the enterocytes differ in young and old individuals, and that the intermitotic cells have age-dependent properties as well. In addition, we could prove that intermitotic cells have a nongrowth fraction, too, which at an advanced age, decreases only slightly although significantly in terms of statistics. For the easily vulnerable crypt epithelium it is a reserve capacity and can b included in the proliferating pool if necessary.

Age Factors↗