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PubMed1986

Comparison of a tumour-derived form of intestinal alkaline phosphatase with foetal and adult intestinal alkaline phosphatases.

An intestinal alkaline phosphatase-like (Kasahara) isoenzyme has been isolated from the serum of a patient with lung cancer and compared with foetal intestinal alkaline phosphatase from the serum of a premature infant and with adult intestinal phosphatase isolated from serum in the same way. Although the ligand-binding sites of the three enzymes were indistinguishable, the foetal intestinal and Kasahara isoenzymes differed slightly from the adult isoenzyme in heat stability and markedly in electrophoretic mobility and neuraminidase-sensitivity, while themselves being similar in these respects. Neither the Kasahara isoenzyme nor foetal phosphatase reacted with anti-placental phosphatase monoclonal antibodies. These results suggest that the Kasahara isoenzyme corresponds to the reappearance of foetal intestinal alkaline phosphatase, rather than to modification of the adult intestinal isoenzyme.

Adult↗
PubMed1986

Intestinal kallikrein activity is reduced in a bypassed segment of the small intestine in the rat.

The possible pancreatic origin of intestinal kallikrein was studied in a jejuno-ileal bypass model in the rat. The bypassed loops were made of variable lengths (2-72 cm) and samples were taken at 10 cm intervals to relate enzyme activities to adaptive changes caused by local and systemic stimulus. The kallikrein activity was dramatically reduced (mean 92.3%) in the bypassed loops while only moderately reduced (mean 35.8%) activities were found in the intestine remaining in continuity. Kallikrein was uniformly distributed throughout the functional small intestine in normal and bypass operated animals. The longitudinal distribution profiles obtained for brush border enzymes in normal animals were almost absent in the bypassed loops, but were apparent in the remaining intestine. The main adaptive growth was observed in the remaining small intestine, Both here and in the loop, the growth depended on the amount of bypassed tissue. Our observations are strongly in favour of a pancreatic origin of the glandular kallikrein activity found in the small intestine in the rat.

Animals↗
PubMed2004

Prolongation of the intestinal viability using oxygenated perfluorocarbon in an experimental model of acute intestinal ischemia.

OBJECTIVES: Liquid perfluorocarbons (PFCs) are well known for their capability to carry respiratory gases. The aim of this study was to evaluate the effectiveness of oxygenated F-Decalin on the intestinal viability, in an experimental model of acute intestinal ischemia. MATERIAL AND METHODS: Thirty-six rabbits were subjected to 8h intestinal ischemia by ligation of the superior mesenteric artery (subgroups 1), the mesenteric vein (subgroups 2) or both vessels (subgroups 3). The animals were divided into three groups: (a) Control (ischemia alone), (b) PFC-O2 (ischemia plus infusion of oxygenated F-Decalin) and (c) PFC (ischemia plus infusion of not-oxygenated F-Decalin). Intestinal biopsies from four different sites and blood samples for serum enzymes measurements were taken at 2, 4, 6 and 8 h. All tissue sections were examined blindly under light microscope. Sections from the specimens were taken at 4 and 8 h, and examined blindly under the electron microscope. Statistical analysis was performed by non-parametric Kruskal Wallis test. RESULTS: Using light microscope, the observed intestinal damages to the sections from Control and PFC groups were severe at 4 h and destructive after 8 h. On the contrary, minimal injuries were observed in the biopsies from PFC-O2 group at 4 and even after 8 h of ischemia. These findings were confirmed by the electron microscope study and correlated to the serum enzymes measurements. CONCLUSIONS: These results suggest that intestinal viability could be prolonged after acute ischemia using oxygenated perfluorocarbons and this could be a promising pretreatment modality for a variety of mesenteric ischemic forms.

Acute Disease↗
PubMed2004

Plasma intestinal fatty acid binding protein (I-FABP) concentrations increase following intestinal ischemia in pigs.

Intestinal fatty acid binding protein (I-FABP) is an intracellular epithelial protein in the intestinal mucosa of many animals. I-FABP appears in the circulation following epithelial damage, and in humans, is proven to be a parameter for damage to the mucosa. In this paper, an ELISA test designed for human I-FABP analysis was used to assay pig blood samples. The test recognized I-FABP cloned from pig small intestine and expressed in Escherichia coli. Furthermore, in our experimental model of (low flow) intestinal ischemia and reperfusion a significant rise in plasma I-FABP concentrations 15-30 min after clamping of the mesenteric artery was demonstrated. This is the first report that in pigs circulating I-FABP is a useful marker for (mild) intestinal injury, and could possibly be used to monitor (intestinal) health in clinical practice.

Animals↗
PubMed2005

Induction of IL-6 within the rodent intestinal muscularis after intestinal surgical stress.

BACKGROUND: Postoperative ileus is a poorly understood surgical problem characterized by leukocyte extravasation into the intestinal muscularis and suppression in muscle function. The study objective was to delineate a mechanistic inflammatory cascade initiated by intestinal manipulation. METHODS: ACI and Sprague-Dawley rats, and IL-6 +/+ and IL-6 -/- mice were subjected to intestinal manipulation. One group of rats received adhesion molecule-blocking antibodies (1A29 and WT.3) before intestinal manipulation. Interleukin-6 (IL-6) messenger RNA (mRNA) levels and electrophoretic mobility shift assay for signal transducers and activators of transcription (STAT) activation were measured in tissue extracts. IL-6 protein levels were assessed by immunohistochemistry and enzyme-linked immunosorbent assay. RESULTS: IL-6 mRNA from muscularis extracts demonstrated a significant induction after intestinal manipulation. No IL-6 induction was observed in mucosal extracts. Adhesion molecule blockade resulted in a marked decrease of cellular infiltration but did not change IL-6 mRNA expression in muscularis extracts. Resident macrophages in the muscularis stained for IL-6 by immunohistochemistry after intestinal manipulation. The isolated manipulated muscularis demonstrated a significant increase in IL-6 release. Electrophoretic mobility shift assay of manipulated muscularis showed a marked increase in IL-6-dependent Stat3 activation. CONCLUSIONS: This study demonstrates that manipulation of the small bowel during an abdominal operation initiates downstream induction, translation, release, and functional activity of IL-6 within the muscularis.

Animals↗
PubMed1988

Evidence for the expression of a primitive intestinal-like alkaline phosphatase in the intestinal 407 cell line.

Intestinal-like alkaline phosphatase was found to be expressed in the intestinal 407 cell line. This enzyme was identified by use of monoclonal antibodies specific for human placental (H7 and HPMS-1) and intestinal alkaline phosphatase (2HIMS-1 and 2HIMS-3) separately. Purification of this isozyme by use of two different monoclonal antibody immunoaffinity chromatographies demonstrates a single protein band on SDS-polyacrylamide gel electrophoresis indicating that this enzyme is not formed as a heterodimer. The apparent monomer subunit molecular weight and the dimer molecular weight of this isozyme were determined to 70000 and 160000, respectively. The enzyme is a homodimer according to molecular weight determinations. Furthermore, this isozyme is neuraminidase sensitive and comparatively heat stable, properties also characteristic for the placental enzyme. Our data suggest that the intestinal-like alkaline phosphatase in the intestinal 407 cell line displays properties intermediate of the intestinal and placental isozymes which may reflect the existence and reexpression of a new primitive isozyme.

Alkaline Phosphatase↗
PubMed1997

The tumor-derived fetal-intestinal alkaline phosphatase cDNA is identical in sequence to the adult intestinal alkaline phosphatase isozyme gene.

The alkaline phosphatase (AP) of Caco-2 cells, a cell line derived from a human adenocarcinoma of the colon, is quite similar to fetal intestinal AP in its enzymatic properties. The nucleotide sequence of a cDNA encoding AP produced in Caco-2 cells was examined. The sequence was identical to one of the three sequences of adult intestinal AP reported previously. We further investigated the entire nucleotide sequence of cDNA of intestinal-type AP produced in cancer cell lines such as HuH-7 cells, FL-amnion cells, and HuG-1 cells. The sequence of these cell APs was identical to that of Caco-2 cell AP. These results indicate that cancer cells producing intestinal-type AP have the same nucleotide sequence as that of adult intestinal AP, and suggest that the differences in electrophoretic mobilities of these cell APs compared with adult intestinal AP may be due to post-translational modifications.

Adult↗
PubMed1999

Abnormalities of enteric neurons, intestinal pacemaker cells, and smooth muscle in human intestinal atresia.

BACKGROUND/PURPOSE: Intestinal dysmotility, which usually has been encountered in the severely dilated proximal segment, is an important problem in postoperative management of patients with intestinal atresia (IA). Changes of enteric nerves had been histochemically examined in both the proximal and distal segments of IA, but a systemic immunohistochemical analysis is still lacking. The aim of this study was to examine precisely alterations of neuronal and muscular elements and pacemaker cells in intestines from patients with IA. METHODS: Resected intestines were obtained from 5 patients with ileal atresia, 3 patients with jejunal atresia, and 3 controls without gastrointestinal diseases (congenital diaphragmatic hernia). All specimens were immunochemically stained with a monoclonal antibody to alpha-smooth muscle actin (SMA) as a smooth muscle marker, polyclonal antibodies to protein gene product (PGP) 9.5 as a general neuronal marker, and to c-kit protein as a maker of intestinal pacemaker cells. In addition, all specimens also were stained by NADPH-diaphorase (NADPH-d) to know the distribution of inhibitory nitrergic nerves. RESULTS: A hypoplasia of the myenteric ganglia and a marked reduction of intramuscular nerve fibers, including nitrergic neurons, were observed in the dilated proximal segment of IA. C-kit-positive cells were localized around the myenteric plexus, but rarely found within the muscularis propria in the proximal segment. The distribution of nerves and c-kit-positive cells in the distal segment was comparable with that seen in controls. A reduced staining intensity for alpha-SMA was mainly observed in the hypertrophic circular muscle layer of the proximal segment. CONCLUSIONS: A hypoplasia of intramural nerves and pacemaker cells was seen predominantly in the proximal segments of IA. Hypertrophy and reduced immunoreactivity for alpha-SMA also were observed in the circular muscle layer of the proximal segment. These alterations of the proximal segment may thus contribute to the postoperative intestinal dysmotility in IA cases.

Actins↗
PubMed2003

Intestinal graft versus native liver cytokine expression in a rat model of intestinal transplantation with and without donor-specific cell augmentation.

BACKGROUND: Immunomodulatory strategies such as donor-specific bone marrow or blood transfusions have been used to promote engraftment after intestinal transplants. We previously showed that delivery of donor antigen via the portal vein can effectively reduce the rate of intestinal graft rejection. The purpose of our current study was to investigate the impact of donor-specific cell augmentation (blood versus bone marrow) via the portal vein on cytokine expression in intestinal grafts versus native livers. MATERIAL AND METHODS: We performed heterotopic small intestinal transplants between male Brown-Norway (donor) and female Lewis (recipient) rats. We studied 10 groups according to the type of donor-specific cell augmentation and the use and dose of immunosuppressive therapy. For cell augmentation, donor-specific blood or bone marrow was transfused via the donor portal vein immediately before graft implantation. For immunosuppression, tacrolimus was used post-transplant at a high or low dose. Control rats received neither immunosuppression nor cell augmentation. Tissue samples for histological assessment were obtained at designated time points. RNA was extracted from intestinal graft and native liver biopsies for cytokine measurements (IL-1 alpha, IL-1 beta, IL-2, IL-4, IL-5, IL-6, IFN-gamma, TNF-alpha, and TNF-beta). Chimerism levels were determined using Q-PCR analysis. RESULTS: Without concurrent immunosuppression, neither portal donor-specific blood nor bone marrow transfusion reduced the rate of rejection. With immunosuppression, outcome was significantly better after portal donor-specific blood (versus bone marrow) transfusion. Irrespective of the type of donor-specific cell augmentation, severe rejection caused strong cytokine expression in the grafts of IL-1 alpha, IL-1 beta, IFN-gamma, and TNF-alpha; in the native livers, mainly of TNF-alpha (with IFN-gamma showing hardly any increase). In general, rejection caused stronger cytokine expression in the grafts than in the native livers. Mild rejection correlated well with strong intragraft expression of IL-6, TNF-alpha, and TNF-beta (early rejection markers); severe rejection with IL-1 alpha, IL-1 beta, IFN-gamma, and TNF-alpha (late rejection markers). In addition to cell augmentation per se, the type of cell augmentation also had an impact on cytokine expression in both grafts and native livers. Cell-augmented (versus tacrolimus-treated) rats showed hardly any differences in intragraft cytokine expression, but the expression of almost all cytokines was significantly stronger in the native livers. With immunosuppression, bone marrow infusion increased intragraft cytokine expression of IL-1 alpha, IL-1 beta, IFN-gamma, and TNF alpha, as well as liver cytokine expression of IL-1 beta, compared to blood transfusion. This finding reflected the more advanced rejection stages in the bone marrow infused group; different types of donor-specific cell augmentation had similar effects on liver cytokine expression. In the absence of myoablative therapy, chimerism levels were low, in both cell-augmented and non-cell-augmented groups. CONCLUSIONS: Rejection and donor-specific cell augmentation independently causes differences in intragraft versus native liver cytokine expression after intestinal transplants. Portal donor-specific blood transfusion, as compared with donor-specific bone marrow infusion, lowered the incidence of rejection and diminished intragraft cytokine up-regulation.

Animals↗
PubMed2002

Evaluation of superporous hydrogel (SPH) and SPH composite in porcine intestine ex-vivo: assessment of drug transport, morphology effect, and mechanical fixation to intestinal wall.

The objective of this study was to investigate the potential of superporous hydrogel (SPH) and SPH composite (SPHC) polymers to enhance the transport of N-alpha-benzoyl-L-arginine ethylester (BAEE) and fluorescein isothiocyanate-dextran 4400 (FD4) across porcine intestinal epithelium ex-vivo, and to study any possible morphological damage to the epithelium by applying these polymers. In addition, the ability of these polymers to attach to the gut wall by mechanical pressure was examined by using a specifically designed centrifuge model. The transport of BAEE and FD4 across the intestinal mucosa was enhanced 2- to 3-fold by applying SPHC polymer in comparison to negative control. No significant morphological damage was observed by applying these polymers inside the intestinal lumen. Moreover, the SPH and SPHC polymers were able to attach mechanically to the intestinal wall by swelling and did not move in the intestinal lumen even when a horizontal force of 13 gms(-2) was applied. In conclusion, these polymers are appropriate vehicles for enhancing the intestinal absorption of peptide and protein drugs.

Animals↗
PubMed1998

Characterization of the regional intestinal kinetics of drug efflux in rat and human intestine and in Caco-2 cells.

PURPOSE: The aim of the present study was to investigate the transport kinetics of intestinal secretory processes in the jejunum, ileum and colon of rats and humans and in Caco-2 cells, in vitro. METHODS: Etoposide, vinblastine sulphate and verapamil hydrochloride were chosen as model substrates since they have been reported to undergo efflux in various other tissues. The concentration dependence, inhibition, directionality, temperature dependence, proton/sodium dependence, and ATP dependence of efflux were studied using side-by-side diffusion chambers and brush border membrane vesicles (BBMVs). Intestinal tissue from rats and humans and Caco-2 cells (passage no. 26) were used. Directional steady state effective permeabilities were calculated from drug appearance in the apical (AP) or basolateral (BL) chambers. Kinetic studies were carried out by investigating substrate efflux at concentrations ranging from 0.2 microns to 1000 microns. Since substrate efflux may be a result of more than one transporter, the hybrid efflux Km (Michaelis-constant), Pc (carrier-mediated permeability), and Pm (passive permeability) were determined as a function of intestinal region. Inhibitor studies were performed using quinidine (0.2mM), a mixed inhibitor of P-glycoprotein (Pgp) and Multidrug Resistance-Associated Protein (MRP), and Leukotriene C4 (100 nM), an inhibitor of MRP and the canalicular multispecific organic anion transporter (cMOAT). Temperature dependent efflux was determined by investigating the BL to AP transport at temperatures ranging from 3 degrees C to 37 degrees C. Energies of activation (Ea) were determined from an Arrhenius analysis. Sodium, proton, and ATP dependence were determined using BBMVs. Immunoquantitation of Pgp, MRP and Lung Resistance Protein (LRP) in Caco-2 cells were carried out using Western blot analysis. RESULTS: Active efflux of all substrates was observed in all regions of rat and human intestine and in Caco-2 cells. Directionality was observed with BL to AP transport exceeding AP to BL transport. The BL to AP/AP to BL permeability ratio, the efflux ratio, ranged from 1.4 to 19.8. Ileal efflux was significantly higher (p < 0.001) than in other regions. Kinetic studies revealed that hybrid efflux Km values ranged from 4 to 350 microns. In some cases, efflux was not saturable due to the solubility limits of the compounds utilized in this study. In presence of inhibitors, efflux ratios approached 1. BL to AP transport was temperature dependent in rat ileum for all substrates. Each of the intestinal efflux was found to be 11.6, 8.3, and 15.8 kcal/mole for etoposide, vinblastine and verapamil, respectively, suggesting an active, energy-dependent efflux mechanism. Substrate efflux was not sodium or proton dependent but was dependent on ATP. Using Western blot analysis the presence of Pgp, MRP, and LRP was demonstrated in Caco-2 cells and the amount of each transport protein varied as a function of passage number. CONCLUSIONS: Using multiple putative efflux substrates, the current results demonstrate that intestinal efflux was regionally dependent, mediated by multiple efflux transporters, the Km's were in the micro-molar range, and involved an energy dependent mechanism(s).

Adenosine Triphosphate↗
PubMed1999

Experimental study of the influence of intestinal flora on the healing of intestinal anastomoses.

BACKGROUND: The beneficial effects of the normal intestinal flora on wound healing in the skin have already been confirmed, and this study attempted to elucidate the influence of the intestinal flora on the healing process in intestinal anastomoses. METHODS: Five groups of rats were studied: germ-free, conventional, monocontaminated with Lactobacillus acidophilus La5 or Escherichia coli X7 and ex-germ-free (conventionalized). All animals underwent ileal and colonic resections followed by anastomoses. Seven days later they were killed and the bursting pressure and hydroxyproline concentration of the anastomoses were measured. The microbiological status of the animals was confirmed weekly. RESULTS: No bacteria were detected in the germ-free rats and no other bacteria were found in the monocontaminated animals. Conventional rats had a significantly higher anastomotic bursting pressure both in the ileum compared with rats monocontaminated with L. acidophilus, and in the colon compared with germ-free rats. The ex-germ-free rats also showed a significantly higher bursting pressure than germ-free animals and rats monocontaminated with either L. acidophilus or E. coli in the ileum and colon. CONCLUSION: The presence of the intestinal flora enhanced the healing of intestinal anastomoses. The data suggest that this effect depends on differences in the types of bacteria in the intestine.

Anastomosis, Surgical↗
PubMed1988

Transgenic mice containing intestinal fatty acid-binding protein-human growth hormone fusion genes exhibit correct regional and cell-specific expression of the reporter gene in their small intestine.

The rat intestinal fatty acid binding protein (I-FABP) gene exhibits cell-specific as well as regional differences in its expression within the continuously regenerating small intestinal epithelium. To investigate the underlying mechanisms, we linked portions of its 5' nontranscribed domain to the human growth hormone (hGH) gene and analyzed expression of the hGH reporter in transgenic mice by RNA blot, solution hybridization, and immunocytochemical techniques. Sequences located within 277 nucleotides of the start site of I-FABP transcription are sufficient to limit hGH expression to the intestine. Although the absolute levels of hGH mRNA in the duodenum and proximal jejunum of these transgenic mice were similar to those of I-FABP mRNA, steady-state hGH mRNA concentrations were approximately 100 times lower in their distal small intestine. Addition of nucleotides -278 to -1178 of the I-FABP gene "restored" hGH mRNA concentrations in the distal jejunum and ileum to levels comparable to murine I-FABP mRNA. Serum hGH levels were 1000 times lower in the "short promoter" transgenic mice compared to animals with the "long promoter" transgene, indicating that efficient distal small intestinal hGH expression is required to produce elevated hGH concentrations in serum. The distribution of hGH in villus-associated enterocytes and goblet cells and its lack of expression in the crypts of Lieberkuhn mimicked that of the endogenous I-FABP gene product in all transgenic pedigrees. However, bands of hGH-negative cells extending from the base to the tips of villi were frequently observed in mice that were heterozygous for the short promoter transgene. This mosaic staining was not observed for I-FABP. These data suggest that (i) different cis-acting sequences may be required for complete expression of proximal-distal I-FABP gradients than for recapitulation of its normal crypt-villus tip distribution; (ii) differences may exist in the export pathways of secreted proteins within enterocytes located in various regions of the small intestine; and (iii) there may be subtle genetic differences among various crypt stem cells that can be detected in vivo by observing mosaic patterns of transgene expression along the villus epithelium.

Animals↗
PubMed1997

Intestinal and extra-intestinal tumor multiplicities in the Apc1638N mouse model after exposure to X-rays.

Seven-week-old Apc1638N mice were exposed to a single dose of 5 Gy total-body X-irradiation resulting in a 8-fold increase in the number of intestinal tumors and a reduction of the lifespan to an average of 6 months. The distribution of tumors along the intestinal tract as well as the adenoma/carcinoma ratio, were similar between non-irradiated and irradiated animals. Semi-quantitative PCR analysis of intestinal-tumor DNA revealed that 10 out of 14 tumors had lost the wild-type Apc allele. However, in contrast to spontaneous Apc1638N intestinal tumors in which the LOH event at the Apc locus involves the entire chromosome 18 (1), in 6 out of 10 tumors derived from X-irradiated animals the Apc loss is associated with only a partial intrachromosomal deletion. The remaining tumors have lost all chromosome 18 markers tested. In addition to the intestinal tumors, female Apc1638N mice are susceptible to the development of mammary tumors. Upon X-irradiation, Apc1638N mice show a striking 15-fold increase in mammary tumors. Moreover, Apc1638N mice spontaneously develop other extra-intestinal neoplasia, such as desmoid-like lesions similar to those associated with familial adenomatous polyposis (FAP), the human syndrome caused by germline mutations in the APC gene. Spontaneous desmoid growth is sex-dependent, as male Apc1638N mice develop 3-fold more desmoids than female mice. Interestingly, X-irradiation seemed to increase the number of desmoids per animal nearly twofold only in female Apc1638N mice. Five out of 9 desmoids found in Apc1638N mice exposed to X-ray displayed loss of the wild-type Apc allele.

Alleles↗
PubMed1986

Intestinal metabolism of nitrosamines. 1. Transport and metabolism of six nitrosamines in isolated perfused rat small intestinal segments.

Possible relationships between structure and metabolism of nitrosamines have been investigated in the rat small intestine. Isolated segments of jejunum and ileum were perfused from the luminal side for 2 h with a Tyrode solution containing one of four symmetrical dialkylnitrosamines with 2-5 carbon atoms per side chain, all 14C-labeled at the alpha position, or one of two unsymmetrical nitrosamines, N-nitroso-tert-butylmethylamine and N-nitrosomethylbenzylamine, 14C-labeled in the methyl group. Besides measurement of 14CO2 production and covalent binding of 14C to intestinal tissue, the absorbed fluid (absorbate) as well as the perfusion medium and tissue homogenates were analysed by h.p.l.c. for the presence of polar metabolites to assess the intestinal metabolism of nitrosamines. Neither N-nitrosodiethylamine nor the two unsymmetrical nitrosamines were metabolized to any significant extent. With increasing chain length of symmetrical dialkylnitrosamines small intestinal metabolism increased dramatically. At a concentration of 1 microM up to 60% and 30% of N-nitrosodipropylamine (NDPA) in jejunal and ileal segments, respectively, and greater than 90% of N-nitrosodibutylamine (NDBA) and N-nitrosodipentylamine (NDAA) in both intestinal segments were metabolized during absorption. Metabolites were found also in perfusate and tissue homogenate but generally at lower percentages as compared with the absorbate. With increasing concentrations the percentage of metabolites decreased, the decrease being more pronounced in ileal as compared with jejunal segments. CO2 production and covalent binding were negligible in ileal segments but amounted up to 5-8% and 0.1-0.4% of the dose in jejunal segments perfused with NDPA, NDBA or NDAA. With NDBA and NDAA no concentration-dependent decrease could be observed, the highest amounts of 14CO2 and bound 14C being found at intermediate concentrations. At concentrations below 10 microM metabolic pathways other than alpha-hydroxylation seem to be of greater importance. The toxicological evaluation of the high intestinal first-pass metabolism of NDPA, NDBA and NDAA must await the identification and quantitation of the metabolites formed.

Animals↗
PubMed1993

Intestinal intraepithelial lymphocytes preferentially repopulate the intestinal epithelium.

We have used C.B-17 severe combined immune deficiency (SCID) mice to study the repopulation of intestinal intraepithelial cells in these mice. We have found that intestinal intraepithelial lymphocytes (IELs) injected into SCID mice preferentially repopulate the intestinal epithelium. About 5 weeks after injection we can detect significant numbers of IEL in repopulated SCID mice. Repopulation occurs in approximately 70% of the injected mice and the amount of recovered cells per mouse is variable. The recovered cells are of donor-type origin and exhibit a typical IEL phenotype. The donor-type T lymphocytes that can sometimes be found in other organs of IEL-repopulated SCID mice are generally of low number. They are not stained with antibodies against IEL-specific markers and their phenotypes appear to be more typical for T cells normally found in these sites. In contrast, the intestinal epithelium of SCID mice cannot be efficiently repopulated with lymphocytes using cells of other organs including thymocytes, Peyer's patch lymphocytes, and bone marrow cells. From our data we conclude that intestinal IELs are confined to the intestinal epithelium and possibly contain a precursor-type cell that preferentially regenerates cells of its own population.

Animals↗
PubMed1992

Reduction of intestinal viscosity through manipulation of dietary rye and pentosanase concentration is effected through changes in the carbohydrate composition of the intestinal aqueous phase and results in improved growth rate and food conversion efficiency of broiler chicks.

The effect of dietary rye (0, 200, 400 and 600 g/kg substituting for wheat) and pentosanase concentration (0, 1, 2, 4, 8, 16 g/kg) on weight gain, molecular weight distribution of soluble carbohydrates in the intestinal lumen and lumenal viscosity in broiler chicks was investigated. A 4 x 6 factorial design was used with four replicates per treatment and six birds per replicate pen. Diets were fed from 1 to 19 d of age, at which time body weight, food intake and intestinal viscosity and molecular weight distribution of carbohydrate complexes in proximal and distal gut sections were determined. Weight gain and food conversion efficiency (FCE) improved with increasing pentosanase and decreasing rye concentration. Intestinal viscosity, which rose as digesta passed from the proximal to distal small intestine, fell with pentosanase addition and decreasing rye concentration. Intestinal viscosity, which correlated positively with reduced weight gain and FCE, was in turn correlated with the lumenal concentration of soluble high-molecular-weight carbohydrates (HMC, greater than 500 kDa), which constituted less than 15% of the total lumenal carbohydrate concentration. The arabinose and xylose content of the HMC increased with increasing rye concentration, suggesting that HMC composition in addition to concentration may determine intestinal viscosity. The results indicate that pentosanase isolated from rye by extraction methods may not be representative of those released by digestion.

Animal Feed↗
PubMedDate not supplied

Intestinal transplantation in pediatric patients: a nursing challenge. Part 2: Intestinal transplantation and the immediate postoperative period.

Intestinal transplantation offers new hope to children with intestinal failure and life-threatening complications of parenteral nutrition. As more transplant centers are adding intestinal transplantation to their existing programs, new challenges are presented to nursing professionals. This three-part series will provide information for nursing professionals regarding evaluation for intestinal transplantation, donor preparation, the surgical procedure, immediate postoperative care of the transplant recipient, and long-term care of the intestinal transplant recipient. This article focuses on donor selection and preparation, the surgical procedure for intestinal transplantation, the immediate postoperative course, immunosuppression, rejection, infections, fluid and electrolyte support, and nutrition. The information presented represents the approach taken at University of Nebraska Medical Center/Nebraska Health Systems.

Aftercare↗