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PubMed1989

Intraperitoneal transplantation of microcarrier-attached enterocytes in rats.

The purpose of this study was to determine whether enterocyte transplantation could be used to correct a specific genetic metabolic defect. Bilirubin uridine diphosphoglucuronyl transferase (UDPGT) activity has been demonstrated in normal rat intestinal mucosa. We hypothesized that normal rat enterocyte transplantation may restore the ability of Gunn rats, which lack bilirubin UDPGT, to conjugate bilirubin. Small intestine was resected from normal Wistar rat donors. Enterocytes were harvested and suspended in Dulbecco's modified Eagle's medium with 10 percent fetal calf serum. Isolated enterocytes were attached to collagen-coated dextran microcarriers and transplanted into congeneic Gunn rat recipients. Recipient rats underwent bile duct cannulation after transplantation, and bile was analyzed for bilirubin glucuronides by high-pressure liquid chromatography. Fifty percent of the transplanted rats showed a significant increase in the concentration of bilirubin monoglucuronide and diglucuronide in their bile 4 and 7 days posttransplantation. Recipient rats had well vascularized microcarrier-enterocyte aggregates in the peritoneal cavity. Our method for intraperitoneal transplantation of isolated enterocytes in rats could potentially be used to correct specific enzymatic and metabolic defects.

Animals↗
PubMed1981

Rat enterocyte Na+ transport in vitro. Action of parathyroid hormone and calcitonin.

Parathyroid hormone (PTH) and calcitonin exert well known effects on the renal tubule which are thought to involve specific hormone receptors and adenyl cyclase. In the intestine, it is not clear whether the action of PTH and calcitonin is only indirect or also direct, and their mechanisms of action are much less well established. In the present study, possible direct effects of PTH and calcitonin on Na+ transport in isolated intestinal epithelial cells of rats were investigated. In the presence of bovine PTH (1.2 I.U/ml) in the incubation medium, the Na+ efflux rate constant (oKNa) of isolated enterocytes was significantly reduced when compared to that in control experiments with the hormone vehicle only. The mean depression of oKNa induced by bovine PTH was 26% as compared to the control (100%) and to that induced by ouabain (4.0 mM) which was 44%. No depressant effect of bovine PTH on oKNa was observed when the isolated enterocytes were incubated with ouabain (4.0 mM). Thus, bovine PTH appeared to inhibit the ouabain-sensitive Na+ pump. When incubating the isolated epithelial cells in an EGTA-containing CA2+-free medium, bovine PTH lost its capacity to inhibit oKNa. Thus, the presence of extracellular Ca2+ appeared necessary for the inhibitory effect of bovine PTH. In contrast to its effect on oKNa, bovine PTH induced no change in net Na+ uptake by isolated enterocytes. Moreover, no significant effect on enterocyte Na+ transport could be demonstrated for salmon or porcine calcitonin at two different concentrations in the incubation medium, Neither bovine PTH nor salmon calcitonin induced significant changes in enterocyte cyclic AMP or cycle GMP concentrations. It was concluded that bovine PTH, but not calcitonin, exerted a directed inhibitory effect on the ouabain-sensitive oKNa of isolated rat enterocytes. The effect of bovine PTH occurred without measurable activation of the cyclic nucleotide system but needed the presence of Ca2+ in the incubation medium to be operative.

Animals↗
PubMed1982

Membrane potentials of differentiating enterocytes.

A positional analysis of enterocyte membrane potential has been carried out using in vitro preparations of rabbit distal ileum. Young enterocytes were found to possess a microvillar membrane potential significantly less than that seen in older enterocytes. The length of enterocyte microvilli was also found to be significantly less in younger enterocytes. It is suggested that developmental changes in membrane potential, occurring during the early stages of enterocyte differentiation, probably reflect a changed permeability to ions associated with the establishment of a fully developed microvillar membrane. Other explanations for the observed findings are also considered.

Age Factors↗
PubMed1994

Crypt cell production rate, enterocyte turnover time and appearance of transport along the jejunal villus of the rat.

Intestinal nutrient absorption is subject to adaptation with, for example, diabetes, diet lipid variations (isocaloric semisynthetic diets enriched with saturated (S) or polyunsaturated (P) fatty acids), ileal resection and abdominal irradiation. These models were used in rats to assess dynamic morphology and distribution of amino acid transporter along the villus. The enterocyte migration rate (EMR) was measured using [3H]thymidine; the vincristine metaphase arrest technique was used to determine the crypt cell production rate (CCPR); quantitative autoradiography was used to assess the time and age of enterocytes when the uptake of 1 and 20 mM [3H]leucine and [3H]lysine was initiated along the villus. The enhanced jejunal uptake of nutrients which occurs after a 50% distal enterectomy was associated with a fall in EMR and CCPR, yet the enhanced nutrient uptake which occurs in diabetes is not associated with any alteration in EMR, CCPR, enterocyte transport pool (ETP), i.e., the length of the enterocyte column along with the villus containing amino acid transporter) or expression of transporter along the villus. The reduced uptake of nutrients in rats fed P as compared with S was associated with increased rather than decreased ETP and age of the enterocytes at the tip of the villus. The reduced nutrient uptake which occurs 3 days after abdominal irradiation was associated with increased EMR and CCPR, and reduced ETP and age of enterocytes of the tip of the villus. However, 14 days after irradiation when nutrient transport remains reduced, these parameters have returned to normal. Thus, alterations in nutrient transport may be associated with changes in the dynamic morphology of the intestine, but the two processes are not necessarily interdependent. We speculate that the changes in the dynamic morphology of the intestine, and the changes of amino acid transport which occurs in these models of intestinal adaptation, are independently controlled.

Amino Acid Transport Systems↗
PubMed1988

In vivo induction of gliadin-mediated enterocyte damage in rats by the mannosidase inhibitor, swainsonine: a possible animal model for celiac disease.

Simultaneous feeding of gliadin and swainsonine, an inhibitor of alpha-D-mannosidases, in rats disturbed enterocytic maturation as shown by a marked loss of activities of alkaline phosphatase and gamma-glutamyltransferase. Morphologically, simultaneous treatment with gliadin and swainsonine caused destruction and decreased density of microvilli, as shown by electron microscopy. Neither gliadin nor swainsonine when given alone had significant effects on enterocytic enzyme activities or enterocytic morphology. Binding of enterocytic glycoproteins to both gliadin-Sepharose and concanavalin A-Sepharose was significantly increased in rats treated with swainsonine. Because swainsonine causes the formation of hybrid-type oligosaccharides with a high binding affinity to mannose-specific lectins, the observed alterations of enterocytic maturation and morphology are presumably caused by the increased binding of gliadin to enterocytic glycoproteins. A possible analogy in the etiology of celiac disease is discussed.

Alkaline Phosphatase↗
PubMed1993

Mosaic differentiation of human villus enterocytes: patchy expression of blood group A antigen in A nonsecretors.

BACKGROUND: The authors have shown that a mosaicism of brush border antigens may occur spontaneously on enterocytes of small intestine in human adult-type hypolactasia. The present paper gives another example of spontaneously occurring mosaicism as indicated by the patchy expression of blood group antigens on villus enterocytes. METHODS: Thirty-five individuals were examined by immunomorphological techniques with antibodies against blood group antigens. RESULTS: In 4 of 16 A blood group individuals, the blood group antigens were expressed only in some villus enterocytes. The individuals with this mosaic pattern were all shown to be nonsecretors. The A antigen in the positive enterocytes of these individuals was only present as the ALe(b) structure, whereas ALe(y) and ALe(d) were also present in the secretors. The patches of positive enterocytes were randomly distributed along the villus wall. CONCLUSIONS: A nonsecretor individuals express the blood group antigens only in some villus enterocytes; this mosaicism does not arise from a heterogeneous population of stem cells within the crypts but rather reflects subtle differences in the pattern of differentiation between monoclonally derived epithelial cells on the villus.

ABO Blood-Group System↗
PubMed1992

Isolation of functionally active intraepithelial lymphocytes and enterocytes from human small and large intestine.

A mild purification method has been developed for the isolation of human intraepithelial lymphocytes (IEL) and enterocytes from the same individual. The isolation procedure includes mechanical disruption of the mucosal layer, treatment with reducing agent and sedimentation followed by Percoll gradient centrifugation. Finally, epithelial cells are removed from the IEL fraction using magnetic beads coated with the anti-epithelial antigen monoclonal antibody (mAb) BerEP4. Leucocytes are removed from the enterocyte fraction using magnetic beads coated with mAbs directed against common leucocyte antigen (CD45). Using this procedure IEL and enterocytes have been isolated from apparently normal jejunal, ileal and colonic tissue specimens. Recoveries of IEL were 7 x 10(5), 4 x 10(5) and 1 x 10(5)/cm2 mucosa from jejunum, ileum and colon respectively. 1-2 x 10(6) enterocytes/cm2 mucosa were recovered from small intestine while the corresponding value for colonic biopsies was approximately 2 x 10(5) enterocytes/cm2. The IEL fraction was pure as judged by the low percentages of B cells, macrophages and BerEP4 positive cells (less than 4%) present in the purified fraction. The enterocyte fraction contained less than 2% CD45+ cells. The two cell fractions were viable and expanded in vitro. Enterocytes expanded spontaneously while IEL required initial stimulation with mitogens. The isolation procedure described here will make it possible to study the function of human IEL, interactions between IEL and enterocytes and the role of both cell types in local immunity.

Adult↗
PubMed1992

Basement membrane components enhance isolated enterocyte growth.

Isolated enterocyte transplantation may have a potential role in increasing intestinal surface area. However, enterocytes are notoriously difficult to grow. Basement membrane components (BMC) promote adherence, migration, and differentiation of enterocytes. Our aim was to determine if BMC enhance enterocyte growth. Twenty-nine rabbits had 5-cm ileal segments resected and serosal pouches (n = 22) created from the serosal surface of the colon. Harvesting of enterocytes by warm trypsinization resulted in 92 +/- 6% cell viability and yielded 5.0 +/- 2.4 10(6) enterocytes/cm intestine. Enterocytes (10(5) were cultured in vitro (n = 7) in 10 ml growth media in plain flasks and flasks coated with laminin alone or Matrigel (an extract of mouse basement membrane containing laminin plus Type IV collagen and heparan sulfate). The cells were subcultured at 2 weeks and examined after Geimsa staining at 4 weeks. Epithelial growth was confirmed by light microscopy and staining for cytokeratin and quantitated by image analysis (JAVA). Epithelial coverage of the flasks was greater with Matrigel (80 +/- 15%) than laminin (66 +/- 15%) which was greater than control (44 +/- 20%) (P less than 0.01). For in vivo studies 10(5) harvested cells were infused into the serosal pouches either in growth media (n = 9) or media + Matrigel (n = 13). Epithelial growth in the pouch was evaluated by qualitative scoring of cytokeratin staining. Cytokeratin staining was similar on control colon serosa (n = 5) and serosa after infusion of cells in media alone. However, Matrigel significantly enhanced the area, depth, and intensity of staining.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Glucose, glutamine, and ketone-body metabolism in human enterocytes.

Suspensions of metabolically viable human small-intestinal epithelial cells (enterocytes) were used to assess the metabolism of substrate(s) normally derived from the blood circulation to the intestinal mucosa (glucose, glutamine, and ketone bodies). Glutamine, glutamate, and glucose were the only substrates that caused major increases in oxygen consumption by isolated human enterocytes. In human enterocytes 72% of glucose could be accounted for as lactate. Human enterocytes utilized glutamine at about 14.90 mumol/min/g dry wt, with glutamate, alanine, aspartate, and ammonia as the major end-products. Human enterocytes utilized 3-hydroxybutyrate and acetoacetate at similar rates. Under the experimental condition employed, the respiratory fuels of human enterocytes include glutamine, glucose, and to a lesser extent, ketone bodies as indicated in the proportion of oxygen consumption attributed to these fuels and to the extent of utilization.

Acetoacetates↗
PubMed1991

Galactose effects on enterocyte differentiation in the mouse jejunum.

The present work investigates the ability of galactose to affect enterocyte differentiation during normal development in vivo. Energy intake has also been varied to take account of the fact that galactose is poorly metabolized in mice. Brush-border lactase, alpha-glucosidase, dipeptidylpeptidase-IV, aminopeptidase N, alkaline phosphatase and microvillus length were measured as markers of enterocyte differentiation in mice fed diets containing galactose (G diet), corn oil (E diet) or galactose + corn oil (G + E diet). Maintaining mice on a G instead of E diet reduced brush-border lactase activity and enterocyte migration rates; alpha-glucosidase, dipeptidylpeptidase-IV, aminopeptidase N and microvillus length expression increased and alkaline phosphatase activity remained unchanged. Feeding the G + E diet restored enterocyte migration rates, lactase, aminopeptidase N and dipeptidylpeptidase-IV activities to values found in mice fed the E diet. Galactose stimulation of alpha-glucosidase and microvillus length expression was, however, fully maintained in mice fed the G + E diet. Present results show that enterocyte differentiation is affected independently by varying dietary galactose and energy levels; that galactose effects always increase and energy effects usually decrease expression of enterocyte components and that energy stimulation of lactase activity is exceptional.

Animals↗
PubMed1986

Testing the hypothesis that crypt size determines the rate of enterocyte development in neonatal mice.

Pieces of mid-jejunum taken from 7-9 day old mice have been used to determine microvillus length in enterocytes located at different points along the crypt-villus axis to test the hypothesis that enterocyte development of structure is directly determined by the physical characteristics of the intestinal crypt. Parallel measurements of enterocyte migration rate were carried out using tritiated thymidine to determine the time course of microvillus elongation in neonatal mice. Microvillus length approximately doubled during early enterocyte migration from the crypt base to the lower part of the villus. Enterocyte migration rate was only 0.9 micron/hr at this stage of development, a value considerably less than that found in adult intestine. Results plotting the time dependency of microvillus elongation were fitted by a logistic curve giving a maximal rate for microvillus growth of 0.004 micron/hr. The corresponding estimate of crypt depth was 35 microns. Both these values are considerably less than those found in adult intestine. These results provide strong support for the general hypothesis that some factor associated with the physical length of the crypt, called crypt factor or CF, is directly responsible for controlling the way enterocytes organize subsequent structural differentiation of their surface membranes.

Aging↗
PubMed1999

The expression and activation of EGF and c-NEU receptors are increased in enterocytes during intestinal adaptation.

BACKGROUND/PURPOSE: After massive small bowel resection (SBR), epidermal growth factor (EGF) and its intestinal receptor (EGF-R) play major roles during adaptation. The expression of a homologous enterocyte receptor termed c-neu (c-neu-R) is capable of forming heterodimers with EGF-R to facilitate cellular signaling. The purpose of this study was to determine the expression and activation of EGF-R and c-neu-R during the adaptive intestinal response to SBR. METHODS: Male ICR mice underwent either SBR or sham surgery. After 1, 3, and 7 days, enterocytes were isolated and protein immunoprecipitated with antibody to either EGF-R or c-neu-R. Receptor protein expression and activation status were determined. RESULTS: When compared with sham operation, the expression and activation status of both EGF-R (six- and twofold, respectively) and c-neu-R (nine- and twofold, respectively) were increased substantially in enterocytes from the adapting ileum after SBR by postoperative day 3. Minimal changes were appreciated for either EGF-R or c-neu-R expression or activation in the remnant bowel after enterocyte removal, liver, or kidney. CONCLUSIONS: Both the expression and activation status of EGF-R and c-neu-R are increased substantially in enterocytes from the adapting ileum by postoperative day 3 after massive SBR. These changes provide a unique mechanism for the enterocyte to enhance cellular signaling in response to EGF during intestinal adaptation.

Adaptation, Physiological↗
PubMed1997

Histidine and histamine metabolism in rat enterocytes.

To study the metabolic fate of L-histidine and histamine in rat isolated enterocytes, enterocytes were incubated in the presence of 0.1 mM L-[U-14C] histidine. At the rate of 11.1 +/- 2.7 pmol/10(6) cells/30 min, the amino acid was incorporated into cellular proteins. 80 microM cycloheximide, i.e. a protein synthesis inhibitor, inhibited this incorporation by 70 +/- 17%. L-histidine was used for cellular protein synthesis which depended on time and concentration. 0.1 mM L-[U-14C] histidine was little oxidized by intestinal cells, i.e. 0.12 +/- 0.06 pmol/10(6) cells/30 min, and was not converted into histamine. When 10 mM histamine was added to the incubation medium, it completely inhibited the incorporation of 0.1 mM [1,4-14C] putrescine into isolated enterocytes. In enterocyte homogenates, this corresponded to inhibition by histamine of putrescine incorporation as catalyzed by transglutaminase activity. Since histamine incorporation into TCA-precipitable material derived from enterocyte homogenates depended on time and concentration, we concluded that exogenous, but not de novo-formed histamine was able to compete with putrescine incorporation into enterocytes as catalyzed by transglutaminase activity.

Animals↗
PubMed1990

Dual mechanisms of inhibition of the immune response by enterocytes isolated from the rat small intestine.

Antigen presentation by enterocytes isolated from the rat small bowel was studied by using T cell proliferation, and immunoregulatory function in an antigen-driven culture system, as indicator systems. Lymph node T cells obtained from rats immunized with ovalbumin (OA) failed to divide when cultured for 4 days in the presence of freshly isolated Ia+ enterocytes and OA. However, cell division was noted when enterocytes were removed after 18 h by Percoll gradient centrifugation, followed by culture of T cells for a further 4 days in the absence of antigen. The failure to divide in the primary culture was due to the secretion by enterocytes of a dialysable non-specific inhibitor. Antigen presentation by enterocytes was specific and was inhibited by monoclonal mouse anti-rat Ia antibody, OX6. An epithelial cell line (REC-2) was established from normal rat small intestine. These cells expressed Ia molecules following incubation with Concanavalin-A stimulated spleen cell supernatant, and were capable of both presenting antigen, and inducing interleukin-2 (IL-2) production, when cultured with primed T cells. Furthermore, Ia+ REC-2 cells functioned as stimulators in a primary mixed lymphocyte reaction (MLR). Both OA-primed T cells activated by enterocytes and antigen, and allogeneic MLR-activated T cells, mediated suppression which was not specific for the initiating antigen. These experiments indicated two mechanisms mediate suppression of cell division in gut mucosa. The contribution of these mechanisms to the control of inflammation at mucosal sites requires investigation.

Animals↗
PubMed1997

gamma-Ray-induced apoptosis in transgenic mice with proliferative abnormalities in their intestinal epithelium: re-entry of villus enterocytes into the cell cycle does not affect their radioresistance but enhances the radiosensitivity of the crypt by inducing p53.

The radiosensitivity of proliferating crypt epithelial cells makes the gut a major limiting factor in the use of radiotherapy for treatment of abdominal cancers. As post-mitotic epithelial cells migrate from mouse small intestinal crypts to the base of adjacent villi, they rapidly lose their ability to undergo apoptosis in response to ionizing irradiation (IR). To determine whether this radioresistance reflects withdrawal from the cell cycle, we used a lineage-specific promoter to direct expression of wild type Simian virus 40 T antigen (SV40 TAg(Wt)) to villus, but not crypt, enterocytes in FVB/N transgenic mice. SV40 TAg(Wt) induced, pRB-dependent, re-entry into the cell cycle is not associated with the acquisition of IR-stimulated apoptosis 4 h or 24 h after 6 Gy or 12 Gy of gamma-irradiation. Co-expression of SV40 TAg(Wt) and K-ras(val12) produces dysplasia in cycling villus enterocytes but no shift towards apoptotic responsiveness to IR. These findings suggest that the radioresistance of villus enterocytes is not simply due to their cell cycle arrest and may be a reflection of their microenvironment. Remarkably, reentry of villus enterocytes to the cell cycle increases the radiosensitivity of the crypt epithelium without changing Bcl-2, Bcl-xL, Bak, or Bax expression. This effect is only manifest after IR and, based upon results obtained with mutant SV40 TAgs, depends upon reaching a critical level of proliferation in villus enterocytes. Like the normal crypt response to IR, the villus-derived enhancement of IR-stimulated crypt apoptosis is associated with an induction of p53 and Raf-1, and is dependent upon p53. Unlike the normal crypt response to IR, the p53 induction involves cells distributed throughout the crypt and the apoptotic response is not confined to the lower half of the crypt. These results indicate that signals initiated by cycling enterocytes can be transmitted to the crypt epithelium to induce p53 and influence their IR-induced apoptosis. Understanding the underlying signaling pathways may provide clues about how to modify a normal crypt's radiosensitivity for therapeutic benefit.

Animals↗
PubMed1994

Synthesis of citrulline from glutamine in pig enterocytes.

The synthesis of citrulline from glutamine was quantified in enterocytes from pre-weaning (14-21 days old) and post-weaning (29-58 days old) pigs. The cells were incubated at 37 degrees C for 30 min in Krebs-Henseleit bicarbonate buffer (pH 7.4) containing 0, 0.5, 2 and 5 mM glutamine. Oxygen consumption was linear during the 30 min incubation period. The rates of citrulline synthesis were low or negligible in enterocytes from 14-21-day-old pigs, but increased 10-20-fold in the cells from 29-58-day-old pigs. This marked elevation of citrulline synthesis coincided with an increase in the activity of pyrroline-5-carboxylate synthase with the animal's post-weaning growth. In contrast, decreases in the activities of phosphate-dependent glutaminase, ornithine aminotransferase, ornithine carbamoyltransferase and carbamoyl-phosphate synthase were observed as the age of the pigs increased. The concentrations of carbamoyl phosphate in enterocytes from pre-weaning pigs were higher than, or similar to, those in the cells from post-weaning pigs. It is possible that the low rate of citrulline synthesis from glutamine in enterocytes from pre-weaning pigs was due to a limited availability of ornithine, rather than that of carbamoyl phosphate. We suggest that this limited availability of ornithine in pre-weaning-pig enterocytes results from (i) the low rate of pyrroline-5-carboxylate synthesis from glutamate, due to the low activity of pyrroline-5-carboxylate synthase, and (ii) the competitive conversion of pyrroline-5-carboxylate into proline. Our present findings on the developmental aspect of citrulline synthesis in pig enterocytes may offer a biochemical mechanism for the previous observations that arginine is a nutritionally essential amino acid for suckling piglets, but not for adult pigs.

Ammonia↗
PubMed1987

Gliadin binding to rat and human enterocytes.

Binding of 125I-crude gluten digest (Frazer's fraction III. FF-III) and 125I-concanavalin A (Con A) to isolated rat enterocytes and of 125I-FF-III to human enterocytes was investigated. Specific binding of 125I-FF-III to rat enterocytes was observed but binding was not inhibited by any of a range of simple and complex saccharides. although casein and bovine serum albumin displaced FF-III at high concentrations. Con A also bound to enterocytes in a specific manner and was inhibited by alpha-methyl-D-mannoside, confirming a lectin-mediated interaction. 125I-FF-III exhibited quantitatively similar specific binding to both normal human and coeliac enterocytes. The primary interaction of gliadin peptides with the enterocyte surface membrane is not lectin-mediated and unlikely to be of fundamental importance in the pathogenesis of coeliac disease.

Animals↗
PubMed1995

Protein synthesis in isolated enterocytes from septic or endotoxaemic rats: regulation by glutamine.

1. We studied the effect of sepsis and the regulation by glutamine of protein synthesis in enterocytes isolated from the small intestine of rats. 2. Sepsis was induced by caecal ligation and puncture; control rats were sham operated. Enterocytes were isolated from the jejunum and incubated in a medium containing [3H]phenylalanine. 3. Sixteen hours after caecal ligation and puncture, protein synthesis, measured as incorporation of radioactivity into protein, was increased by 65%, 89% and 137% respectively in enterocytes from the tips and mid-portions of the villi and from the crypts. 4. Addition of glutamine to incubated enterocytes stimulated protein synthesis in a dose-dependent manner, and this effect was most pronounced in crypt cells from septic rats. The effect of glutamine on protein synthesis was duplicated by equimolar concentrations of acetoacetate or 3-hydroxybutyrate, both of which may serve as fuel for enterocytes, and was blocked by the glutaminase inhibitor 6-diazo-5-oxo-L-norleucine. 5. The results suggest that sepsis stimulates protein synthesis in enterocytes and that glutamine regulates protein synthesis in the same cells, probably by energy provision.

Animals↗