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At least 235 records · Page 13Linked to original sources

PubMed1989

Metabolism of the contraceptive steroid desogestrel by the intestinal mucosa.

1. The intestinal mucosal metabolism of the progestogen oral contraceptive desogestrel (Dg) has been studied in vitro using the Ussing chamber technique. Histologically normal ileum or colon was obtained from eight patients undergoing various resections. The mucosal sheets were mounted between two perspex chambers. 2. Two hours after addition of [3H]-Dg (0.2 microCi; 100 ng) to the mucosal chamber, more than 90% of the steroid was present in that chamber. In studies with colon, metabolite analysis showed that 55.4 +/- 11.7% (mean +/- s.d.; n = 6) of drug present was Dg, 28.9 +/- 11.4% as unconjugated Phase I metabolites, 13.3 +/- 2.6% as sulphate conjugates and 2.5 +/- 1.5% as glucuronide conjugates. 3. By co-chromatography with authentic metabolites and mass spectrometry, it was shown that 3-keto desogestrel is formed in the mucosa. This is the active metabolite of desogestrel. A large peak of radioactivity did not co-chromatograph with any known metabolites and has been tentatively identified as ring hydroxylated products of 3-keto desogestrel. 4. The effect of the synthetic oestrogen ethinyloestradiol (EE2) on the metabolite profile of Dg was studied. In the presence of increasing concentrations of EE2 (100 ng, 1 and 10 micrograms), there was competition for sulphation such that the sulphate fraction decreased by 32, 49 and 48% respectively. 5. The results of this study indicate substantial first pass metabolism of desogestrel by the gut mucosa with evidence for the formation of the active metabolite. The extent of phase I metabolism is unusual.

Chromatography, High Pressure Liquid↗

PubMed1998

Species differences in the disposition of propranolol prodrugs derived from hydrolase activity in intestinal mucosa.

The bioavailability of propranolol (PL) after oral administration of ester-type prodrug was compared in rat and dog, and the possible reason for species difference was investigated. In dog, the oral bioavailability of PL was enhanced by the use of prodrug due to saturation of metabolism of PL. In contrast, high (10 mg/kg) and low (2.5 mg/kg) doses of butyryl PL and isovaleryl PL failed to improve oral bioavailability of PL in rats. The hydrolase activities for prodrugs in rat liver were lower than those of dog (by 4-12-fold), but those of rat intestinal mucosa were significantly higher than those of dog (50-260-fold). Although it is clear from the in vitro hydrolysis using subcellular fractions that the rapid hydrolysis in intestinal mucosa was mainly due to cytosolic components, the brush-border membrane vesicle in rat intestine also showed hydrolase activity for both prodrugs. In situ absorption experiment in rat revealed an improvement in the apparent absorption rate of PL as the result of prodrug use (1.3-fold) and the nearly complete hydrolysis of isovaleryl PL during intestinal absorption, which is a slower hydrolyzed prodrug than butyryl PL in intestinal mucosa and liver. The defects for enhancing oral bioavailability in rats appears to be based on an unsaturation of metabolism for PL, which is derived from a decrease in PL concentration in hepatocytes, owing to rapid hydrolysis of the prodrug in intestinal mucosa and slow hydrolysis of the prodrug in liver. Furthermore, human intestinal mucosa showed a surprisingly high hydrolase activity in microsomes. Therefore, the oral bioavailability of PL after administration of prodrugs might be not significantly improved in human.

Administration, Oral↗

PubMed1980

[Ischemic lesions and post-ischemic regeneration of the small intestinal mucosa].

After ligationof the vascular arcades of the upper jejunum in rats ischemic damage to the intestinal mucosa and its regenerative behavior were investigated by histology, morphometry, enzyme-histochemistrym, autoradiography and electron microscopy. The process of ischemic damage begins at the tips of the villi and progresses to the crypts. After ischemia lasting 300 min the mucosa, submucosa and muscularis propria are necrotic, which means, that the small intestine is at this time completely infarcted. Whilst sthe ischemic damage to the crypt epithelia is similar to that of other kinds of epithelia, the ischemic damage to the enterocytes is different. The enterocytes are shed to the intestinal lumen without any signs of irreversible damage by a blebformation at their cell base. After 2 h ischemia -- the basal epithelia of the crypts are not irreversible damaged yet at this time--and a 12 h period of restored blood flow, the mucosal surface is completely covered again by a flat epithelium. This is achieved 1) by an above-normal proliferation of the epithelia derived from the residual crypts, 2) by the appearance of flat epithelia with an increased diameter. After 8 days of repair the small intestinal mucosa shows morphologically, autoradiographically and enzyme-histochemically a normal picture again.

Acid Phosphatase↗

PubMed2006

Isolation of Helicobacter pylori from the intestinal mucosa of patients with Crohn's disease.

BACKGROUND: Helicobacter species are associated with inflammatory bowel disease in rodents and in nonhuman primates. Therefore, we prospectively investigated the presence of Helicobacter species in the intestinal mucosa of patients with and without Crohn's disease by culture and polymerase chain reaction (PCR) assays. MATERIALS AND METHODS: Mucosal fragments were obtained from the ileum, different colon regions, and rectum of 43 patients with Crohn's disease and of 74 patients without inflammatory bowel disease. RESULTS: Helicobacter pylori strains, identified by 16S rRNA gene sequencing, were more frequently isolated and PCR-detected in the intestinal mucosa of patients with ulcerative colitis-like Crohn's disease than in intestinal mucosa of the control group. Otherwise, anti-H. pylori immunoglobulin G levels were significantly lower in fibrostenosing and fistulating Crohn's disease subgroups. No other Helicobacter species were found in the intestinal mucosa of the patients. CONCLUSIONS: Although our results suggest an association between the presence of H. pylori in the intestine and ulcerative colitis-like phenotype of Crohn's disease, H. pylori infection in the actual causality of Crohn's disease is still to be determined.

Adolescent↗

PubMed2006

Dietary cholecalciferol and phosphorus influence intestinal mucosa phytase activity in broiler chicks.

1. The role of cholecalciferol and phosphorus in the regulation of intestinal mucosa phytase was investigated in broiler chicks. 2. A total of 144 7-d-old male broiler chicks were grouped by weight into 6 blocks of 4 cages with 6 broiler chicks per cage. Four maize-soybean meal-based mash diets were randomly assigned to cages within each block. The 4 diets consisted of cholecalciferol at 0 or 75 microg/kg and total phosphorus at 3.6 or 7.0 g/kg in a 2 x 2 factorial arrangement. The birds were given the experimental diets for 12 d under conditions which excluded ultraviolet light. 3. Broiler chicks fed on diets with the higher concentration of cholecalciferol had higher Vmax and Km of the mucosa phytase, weight gain, feed intake, feed efficiency and percentage tibia ash, higher ileal digestibility of dry matter, energy, phosphorus (P) and calcium (Ca), and increased retention of dry matter, nitrogen, P, Ca and energy. 4. Broiler chicks receiving diets with the higher P concentration showed lower Vmax and Km of the intestinal mucosa phytase but greater weight gain, feed intake, feed efficiency and percentage tibia ash, higher ileal digestibility of dry matter, energy, P and nitrogen, and increased retention of dry matter, energy, nitrogen and Ca. 5. In conclusion, both dietary P and cholecalciferol influenced the activity of intestinal mucosa phytase.

6-Phytase↗

PubMed2003

Effects of nonpathogenic bacteria on cytokine secretion by human intestinal mucosa.

OBJECTIVE: The human intestine harbors a complex microbial ecosystem, and the mucosa is the interface between the immune system and the luminal environment. The aim of this study was to elucidate whether host-bacteria interactions influence mucosal cytokine production. METHODS: Macroscopically normal colonic specimens were obtained at surgery from eight patients with neoplasm, and inflamed ileal specimens were obtained from two patients with Crohn's disease. Mucosal explants were cultured for 24 h with either nonpathogenic Escherichia coli ECOR-26, Lactobacillus casei DN-114 001, L. casei DN-114 056, L. casei ATCC-334, or Lactobacillus bulgaricus LB-10. Each study included blank wells with no bacteria. Tissue and bacteria viability were confirmed by LDH release and culture. Concentration of tumor necrosis factor (TNF)alpha, transforming growth factor beta1, interleukin (IL)-8, and IL-10 was measured in supernatants. In parallel experiments, neutralizing anti-TNFalpha antibody was added to the culture. RESULTS: Co-culture of mucosa with bacteria did not modify LDH release. Co-culture with L. casei strains significantly reduced TNFalpha release, whereas E. coli increased it. These effects were observed both in normal and inflamed mucosa. In combination studies, L. casei DN-114 001 prevented TNFalpha stimulation by E. coli. L. casei DN-114 001 also reduced IL-8 release via a TNFalpha-independent pathway. L. casei DN-114 056 or E. coli increased IL-10 release in the presence of neutralizing anti-TNFalpha. CONCLUSIONS: Nonpathogenic bacteria interact with human intestinal mucosa and can induce changes in cytokine production that are strain specific.

Aged↗

PubMed1998

[Nephrogenic adenoma in intestinal mucosa. A case in urethro-sigmoid anastomosis].

OBJECTIVE: To describe a case of nephrogenic adenoma occurring in the intestinal mucosa of the neobladder urethro-sigmoid anastomosis in a patient who had undergone cystectomy for a bladder carcinoma. METHODS/RESULTS: Of 14 cases of nephrogenic adenoma in 11 patients, one involved the lamina propria of large bowel mucosa. A 67-year-old patient submitted to radical cystoprostatectomy and orthotopic bladder substitution using a detubulized sigmoid neobladder due to multicentric G3 pTa, pTis urothelial bladder carcinoma had two episodes of stricture of the distal anastomosis. After the second episode, endoscopic resection of the area was performed. Histological examination of the specimen disclosed nephrogenic adenoma of the intestinal mucosa. CONCLUSIONS: Nephrogenic metaplasia has been observed in the intestinal mucosa of patients undergoing different urological procedures. To our knowledge, our patient is the third case involving large bowel mucosa reported in the literature. These three cases suggest that nephrogenic adenoma might not be a metaplastic process specific to the urothelium.

Adenoma↗

PubMed1989

The glycosphingolipid composition and glycosyltransferase activities of the small intestinal mucosa of testosterone-treated rats.

Prior studies have demonstrated that sex hormones can influence the glycosphingolipid composition of different organs, including small intestine. However, to date, the effects of testosterone on glycosphingolipids of rat small intestinal mucosa have not been examined. Experiments were conducted to examine the effect of subcutaneous administration of synthetic testosterone (500 micrograms/100 g body wt.) on the gangliosides and neutral glycosphingolipids of rat small intestinal mucosa. Their results demonstrated that testosterone administrations: (i) increased the ganglioside content including hematoside (GM3); (ii) increased the total content of neutral glycosphingolipids, which was due to the increases in glucosylceramide and globotriaosylceramide; (iii) increased the activities of cytidine 5'-monophosphate-N-acetylneuraminic acid: lactosylceramide sialyltransferase, and UDPgalactose: lactosylceramide galactosyltransferase; (iv) increased the percentage of the long chain base phytosphingosine in hematoside, glucosyl-, and globotriaosylceramide; and (v) significantly altered the fatty acid composition of each of these glycosphingolipids. These results demonstrate that administration of testosterone induces alterations in glycosphingolipid composition and glycosyltransferases activities in rat small intestinal mucosa.

Animals↗

PubMed1981

Hypersensitivity reactions in the small intestine. 6. Pathogenesis of the graft-versus-host reaction in the small intestinal mucosa of the mouse.

The intestinal phase of the graft-versus-host reaction (GVHR) has been investigated in adult F1 mice bearing grafts of fetal gut using an H-2-incompatible and an H-2-compatible, Mls-incompatible combination. The results indicate that the mitotic activity of the intestinal crypts and the number of intraepithelial lymphocytes are sensitive parameters of the mucosal cell-mediated immune response in the GVHR. Using these indices, indirect evidence has been obtained that soluble factors may be responsible for the damage to the intestine in the GVHR. Possible pathways of lymphocyte activation and migration to the gut are proposed to explain the role of gut-associated T cells in the production of these mediators.

Animals↗

PubMed1975

Disaccharidases in rat small intestinal mucosa following cytostatic treatment with adriamycin.

Our studies have shown that appropriate doses of adriamycin can reduce the activities of the intestinal disaccharidases in the rat. At higher doses, in addition to morphological changes in the intestinal mucosa, a considerable fall in disaccharidase activities also occurs. This functional impairment can be seen for a period of several days after the morphological restitution of the mucosa. Appropriate studies of the small intestinal mucosa in man will have to be undertaken to show whether similar impairment occurs at therapeutic doses.

Animals↗

PubMed1998

Effects of Echinostoma caproni infection on the phospholipid and sphingolipid content of the intestinal mucosa of ICR mice.

High performance thin layer chromatography (HPTLC) was used to determine phospholipids and sphingolipids in the intestinal mucosa of ICR mice infected with Echinostoma caproni for two weeks. The major phospholipids detected in both infected and non-infected mucosa were phosphatidylcholine (PC) and phosphatidylethanolamine (PE). HPTLC-densitometric analysis showed that there was a significant decrease in the weight of both PC and PE in the intestinal mucosa of infected mice compared to that of the uninfected controls. Cerebrosides and sulphatides, but not sphingomyelin, were identified in the intestinal mucosa of both infected and uninfected hosts. There was an apparent increase in the cerebroside content of the mucosa of infected versus control mice. The pathobiochemical changes seen in the polar lipid content of infected hosts probably reflect the feeding and behavioural activities of E. caproni in the mouse intestine.

Animals↗

PubMed2004

Mesna ameliorates intestinal mucosa damage after ifosfamide administration in the rabbit at a dose-related manner.

BACKGROUND: Cancer chemotherapy may lead to mucositis, a serious dose-limiting side effect. The alkylating agent ifosfamide is used in the treatment of various forms of cancer in combination with the uroprotective thiol mesna (2-mercaptoethane-sulfonate). The aims of this study were to assess the dose response intestinal mucosa damage of ifosfamide and to investigate the potential protective effect of mesna on rabbit intestinal epithelium. MATERIALS AND METHODS: Fifty New Zealand White rabbits were randomly assigned to 10 groups of five animals each and received intravenously every week for 10 weeks either normal saline, ifosfamide, mesna, or ifosfamide plus mesna at three escalating dose levels (ifosfamide: 30, 45, or 60 mg/kg; mesna: 12, 18, or 24 mg/kg divided into two equal doses administered 4 h apart). Intestinal mucosa damage was assessed on the basis of crypt cell apoptosis and proliferation as well as intestinal morphometry. Apoptosis was detected by agarose gel electrophoresis and quantified by the DNA fragmentation assay and a standard terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate-biotin nick-end labeling (TUNEL) method by which the percentage of fragmented DNA and the apoptotic index were determined, respectively. The mitotic index and the crypt-villus (c/v) unit height were also measured in histological sections. RESULTS: Ifosfamide caused a dose-related increase of crypt cell apoptosis and shortening of c/v unit, while it had a steady antimitotic effect. Mesna as a sole agent had no apoptotic or trophic effect on intestinal mucosa and hence no effect on intestinal morphometry. However, mesna, when administered concurrently with ifosfamide, ameliorated apoptosis, hypoproliferation, and mucosal atrophy at a dose-related manner. CONCLUSIONS: Ifosfamide causes intestinal mucosa damage, which may be ameliorated in a dose-related manner by coadministration of mesna.

Animals↗

PubMed1997

The acute infectious diarrhoeas as diseases of the intestinal mucosa.

One of the intriguing aspects of the acute infectious diarrhoeas is that, while resulting from an infection of the intestinal tract, they only last from a few hours to a few days. The study of the interactions between infectious agents and intestinal epithelium has allowed a better understanding of the cellular and molecular mechanisms that cause the sudden loss of water and electrolytes, the hallmark of acute diarrhoea. These interactions have also led to formulating oral rehydration solutions used worldwide now. They do not, however, allow understanding the short course of most intestinal infections. For that, one has to consider the intestinal epithelium as part of an anatomical and functional system that, including the many types of cells present in the lamina propria, constitutes the intestinal mucosa. Infectious agents interact with the whole of the mucosa, including the cells of the lamina propria. This leads, among other things, to a change in the functions of the epithelial cells and accelerates their turnover. The pathophysiology of the intestinal mucosa leads to better understand the short and benign course of most intestinal infections. It also leads to better understand the physiology of the intestinal mucosa, and the interactions between the body and its nutritional environment.

Acute Disease↗

PubMed2005

Epsilon germ-line and IL-4 transcripts are expressed in human intestinal mucosa and enhanced in patients with food allergy.

BACKGROUND: The mechanisms of gastrointestinal (GI) food allergy (FA) are poorly understood. Immunoglobulin E (IgE) is increased in stools from patients with FA, as well as the number of cells carrying IgE in intestinal mucosa, but the origin of IgE production remains unknown. To investigate a local production of IgE in intestine, we analysed the levels of transcripts for epsilon germ-line (epsilonGT), and potential regulators of IgE production, IL-4, IL-13, IFN-gamma, IL-4Ralpha, STAT6 and FcepsilonRIalpha in intestinal mucosa of adult patients with FA. METHODS: Endoscopic biopsies were obtained from the caecum of 25 patients with FA and 14 control patients. The levels of epsilonGT, IL-4, IL-13, IFN-gamma, IL-4Ralpha, STAT6 and FcepsilonRIalpha mRNA were analysed by real-time RT-PCR and compared with unpaired nonparametric Mann-Whitney test. RESULTS: The mean epsilonGT transcript level in caecum was increased in FA patients compared with control patients (P < 0.05). IL-4 mRNA expression was also increased in FA patients (P < 0.05), whereas mRNA expression for IL-13, IFN-gamma, IL-4Ralpha, STAT6 and FcepsilonRIalpha mRNA expression was not altered. However, the ratio of IL-4 mRNA/IFN-gamma mRNA was significantly increased in FA patients (P < 0.05). No correlation was observed between epsilonGT transcripts expression in intestinal mucosa and total IgE levels in serum. CONCLUSIONS: This study shows that (i) epsilonGT transcripts are expressed in human intestinal mucosa; (ii) epsilonGT and IL-4 transcripts are increased in caecal mucosa from patients with FA. These results suggest local production of IgE in intestine that might be of importance for inflammatory reactions in the GI tract.

Adult↗

PubMed1988

Premalignant alterations in the glycosphingolipids of small intestinal mucosa of rats treated with 1,2-dimethylhydrazine.

1,2-Dimethylhydrazine is a procarcinogen with selectivity for the colon and proximal small intestine. In weekly subcutaneous (s.c.) doses of 20 mg/kg body weight, this agent produces colonic and proximal small intestinal tumors in a high percentage of rodents with a latency period of approximately six months. To determine whether alterations in the glycosphingolipid content of rat proximal and/or distal small intestinal mucosa existed before the development of dimethylhydrazine-induced cancer, rat were given s.c. injections of this agent (20 mg/kg body weight per wk) or diluent for five wk. Animals were killed at this time, and mucosa was isolated from each small intestinal segment of both groups. Glycosphingolipids then were extracted from these tissues and analyzed by high performance thin layer chromatography and gas liquid chromatography. The results of these studies demonstrated that (1) the content of neutral and acidic glycosphingolipids was significantly decreased (approximately 20%) in the proximal small intestine of treated rats compared with their control counterparts; (2) no significant difference in the glycosphingolipid content was seen, however, in the distal small intestinal mucosa of control and treated rats; and (3) while significant differences were noted in the majority of fatty acids of GM3, glucosyl- and globotriaosylceramide in the proximal small intestine of control and treated animals, differences in the fatty acids of these glycosphingolipids in the distal segment of these groups were confined to stearic (18:0) acid and/or arachidic (20:0) acid.

1,2-Dimethylhydrazine↗

PubMed1987

Changes in intestinal mucosa above lymph follicles during carcinogenesis in rats. A light and electron microscopic study.

Changes in the intestinal mucosa during carcinogenesis were investigated in 36 rats after weekly s.c. injection of 20 mg dimethylhydrazine/kg bodyweight. More changes were seen in the large than in the small intestine. In the first week, 60% of colonic lymphoid plaques displayed various crypt abscesses and glandular regenerations. These mucosal changes correspond to the glands covering the lymph follicles, in direct contact with lymphoid cells. Beginning in week 8, dysplastic glands developed in these mucosal areas above the lymph follicles. The number of lymphoid plaques with dysplastic glands in the large intestine increased week by week, attaining 75% in week 20. At the end of week 12 the first adenocarcinoma was detected in the cecum by light microscopy, and classified as a poorly differentiated adenocarcinoma with signet ring cells infiltrating the lymph follicles which contained endocrine cells. The majority of adenocarcinomas (10 cases) occurred in week 20. Of these, 7 were localized above the lymphatic plaques in the intestine. Endocrine cells were found in varying numbers in 6 of 10 adenocarcinomas. Three endocrine cell carcinomas, corresponding to human adenocarcinoids or goblet cell carcinoids, developed within the intestinal mucosa; all were identified as poorly differentiated intestinal adenocarcinomas, two of them situated above lymph follicles. These suprafollicular tumors developing from the glandular base, were composed of mucoid cells, endocrine cells, and undifferentiated cells. Microcarcinomas are considered as initial stages of endocrine cell carcinoma.

1,2-Dimethylhydrazine↗

PubMed1999

[Effects of basic fibroblast growth factor on repairing injury of intestinal mucosa in acute necrotic pancreatitis].

OBJECTIVE: To observe the effects of basic fibroblast growth factor (bFGF) on repairing injury of intestinal mucosa in acute necrotic pancreatitis (ANP). METHODS: Sixteen dogs of ANP animal model were made by injection of 5% sodium taurocholate (0.5 ml/kg) with 3,000 U/kg trypsin into the pancreatic duct. The mucosa structure, content of protein, DNA and malondiethylaldehyde (MDA) were observed after ANP and treatment with bFGF, and the plasma lipopolysaccharide and endothelin-1 were detected. The organs of dogs were made to bacterial culture. Ileal mucosa was collected for histological and ultrastructural studies. RESULTS: The results showed that after treatment with bFGF, the injury of intestinal mucosa in ANP was abated. The length, height and area of mucosa microvillus, the content of DNA and protein of ileal mucosa were significantly increased, while the plasma endothelin-1 and lipopolysaccharide were reduced. The organ bacterial translocation rate was also decreased in 50%. CONCLUSION: bFGF has good effects on abating injury of intestinal mucosa, protecting gut barrier function, reducing the incidence of lipopolysaccharide and bacterial translocation after ANP.

Animals↗

PubMed2000

Induction of the stress response increases interleukin-6 production in the intestinal mucosa of endotoxaemic mice.

Previous studies suggest that production of interleukin-6 (IL-6) is increased in the intestinal mucosa during sepsis and endotoxaemia. We tested the hypothesis that mucosal IL-6 production during endotoxaemia is increased further by the heat-shock (stress) response. The stress response was induced in mice by hyperthermia (rectal temperature of 42 degrees C for 3 min) or by intraperitoneal injection of sodium arsenite (10 mg/kg). At 2 h after induction of the stress response, groups of mice were injected subcutaneously with endotoxin (10 mg/kg) or sterile saline. IL-6 mRNA and protein levels in the jejunal mucosa were determined by an RNase protection assay and an ELISA respectively, and levels of hsp72 (heat-shock protein of 72 kDa) were determined by Western blot analysis. Hyperthermia and sodium arsenite increased hsp72 levels in the intestinal mucosa. IL-6 concentrations were increased in the jejunal mucosa of endotoxaemic mice, and this effect of endotoxaemia was potentiated by the stress response. Mucosal IL-6 mRNA levels were increased in endotoxaemic mice, and were increased further by the stress response. Thus it is concluded that mucosal IL-6 production during endotoxaemia may be further stimulated by the stress response. Increased IL-6 levels in the intestinal mucosa may be a potential mechanism by which the stress response exerts a protective effect during sepsis and endotoxaemia.

Analysis of Variance↗