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At least 829 records · Page 46Linked to original sources
PubMed2000

Inhibition of the protective IgA response by ketotifen is related to the inflammatory reaction in the peritoneal cavity and intestinal mucosa of BALB/c mice infected with Trichinella spiralis.

Interleukin-5 (IL-5) production, eosinophilia, and IgA responses of BALB/c mice infected with Trichinella spiralis were measured in the peritoneal cavity and intestinal mucosa. Ketotifen, an anti-allergic compound, was used to control the inflammatory response. IgA responses differed against adult and muscle stages of the parasite and between the intestine and the peritoneal cavity. IL-5 and eosinophil production also differed between the intestine and the peritoneal cavity. The occurrence of parasite-specific IgA antibodies in the peritoneal cavity may reflect the migration of cells from the lamina propria. Following ketotifen treatment there was a reduction in the IL-5, eosinophilic, and IgA responses; these responses affected both the size of worms and the number of worms.

Animals↗
PubMed1977

[Characteristics of the ultrastructural changes of the large intestine mucosa after acute dysentery].

Electron microscopic examinations of biopsy specimens of the large intestine from 8 patients one month after termination of the acute phase of dysentery revealed dystrophic and destructive changes in surface epithelium cells consisting in the lack of glycocalyx, fragmentation of microvilli, vacuolation and subsequent homogenization of the cytoplasm. Swelling and destruction of mitochondria, pyknosis and rhexisof the nucleus, exposure and loss of the intactness of the apical membrane of the cells were observed. The altered colonocytes frequently became detached off the basal membrane, exposing the stroma. The results of the study attest to long-term persistence of both the pathological and infectious processes in protracted forms of Shigella infection in man.

Acute Disease↗
PubMed1980

A kinetic and equilibrium binding study of 1 alpha,25-dihydroxyvitamin D3 with its cytosol receptor from chick intestinal mucosa.

A kinetic and equilibrium binding study of the interaction of 1 alpha,25-dihydroxyvitamin D3 (1 alpha,25-(OH)2D3) with its receptor system from chick intestinal mucosa has been carried out. The equilibrium dissociation constant (Kd) for the binding of 1 alpha,25-(OH)2D3 to the crude cytoplasmic receptor varies from 2.3 x 10(-10) M at 4 degrees C to 5.0 x 10(-10) M at 24 degrees C, yielding values for delta G0, delta H0 and delta S0 for the dissociation process of 12.2 +/- 0.1 kcal/ mol, 6.7 +/- 1.2 kcal/mol, and -19.9 +/- 3.2 cal/degree mol. This suggests that the binding of 1 alpha,25-(OH)2D3 to the receptor may be an entropy-driven process. Kinetic studies on the association and dissociation of the 1 alpha,25-(OH)2D3 . receptor complex revealed that kassoc varied from 0.6 x 10(7) M-1 min-1 at 0 degrees C to 14.5 x 10(7) M-1 min-1 at 30 degrees C and that kdiss varied from 4 x 10(-5) min-1 at 4 degrees C to 4 x 10(-2) min-1 at 30 degrees C. The activation energy for the association process was found to be 17 kcal/mol, while that for the dissociation reaction was 45 kcal/mol.

Animals↗
PubMed2004

Regeneration of injured intestinal mucosa is impaired in hepatocyte growth factor activator-deficient mice.

BACKGROUND AND AIMS: Hepatocyte growth factor activator (HGFA) is a serum proteinase that specifically converts an inactive single-chain form of hepatocyte growth factor (HGF) into an active 2-chain form. HGFA is produced in its precursor form and then activated in injured tissues. To address the precise role of HGFA and to investigate the mechanisms of HGF activation in injured tissues, we generated mice deficient in HGFA. METHODS: HGFA-deficient mice were generated using targeted gene disruption. The regenerating process of intestinal mucosa damaged by oral administration of dextran sodium sulfate (DSS) or by rectal administration of acetic acid was examined in both HGFA-deficient and control mice. HGF processing activity was analyzed using Western blotting and an HGF activation assay. RESULTS: Homozygous mutant mice were viable and fertile without obvious abnormalities. When mice were treated with 3% DSS in drinking water for 6 days followed by distilled water without DSS, 72% of HGFA-deficient mice died through day 12 while 75% of control mice survived injury. Similar results were also observed in the acetic acid-induced intestinal injury; the survival rate was 36.6% in HGFA-deficient mice and 84.2% in control mice. In HGFA-deficient mice, the injured mucosa was not sufficiently covered by regenerated epithelium and the activation of HGF was impaired in the injured colon. CONCLUSIONS: These results indicate that HGFA is required for repair of injured intestinal mucosa but is not essential for normal development during embryogenesis or after birth.

Animals↗
PubMed1986

Adhesion of Candida albicans to mouse intestinal mucosa in vitro: development of the assay and test of inhibitors.

This study describes an in-vitro assay for estimating numbers of Candida albicans adherent to mouse intestinal mucosa. No significant differences were observed in the capacity of C. albicans to adhere to genetically distinct mouse strains nor in the binding ability of three C. albicans strains. Chitin soluble extracts, prepared from chitin isolated from C. albicans or from chitin obtained commercially, inhibited adhesion of the yeasts to duodenal tissue by 48% and 43%, respectively.

Adhesiveness↗
PubMed2002

Are MDCK cells transfected with the human MRP2 gene a good model of the human intestinal mucosa?

PURPOSE: To investigate whether Madin-Darby canine kidney cells transfected with the human MRP2 gene (MDCK-MRP2) are a good model of the human intestinal mucosa. METHODS: MRP2 expression in Caco-2 cells was compared with the expression of this efflux transporter in MDCK-wild type (MDCK-WT) and MDCK-MRP2 cells using Western blotting methods. The polarized efflux activities of MRP2 in the MDCK-MRP2, MDCK-WT. MDCK cells transfected with the human MDR1 gene (MDCK-MDR1), and Caco-2 cells were compared using vinblastine as a substrate. Apparent Michaelis-Menten constants (K(M), Vmax) for the efflux of vinblastine in Caco-2 and MDCK-MRP2 cells were determined in the presence of GF120918 (2 microM), which inhibits P-glycoprotein but does not affect MRP2. Apparent inhibitory constants (K(I)) of known substrates/inhibitors of MRP2 were determined by measuring their effects on the efflux of vinblastine in these cell lines. RESULTS: MDCK-MRP2 cells expressed higher levels of MRP2 than MDCK-WT and Caco-2 cells as measured by Western blotting technique. Two isoforms of MRP2 expressed in Caco-2 and MDCK cells migrated at molecular weights of 150 kD and 190 kD. In MDCK-MRP2 cells, the 150 kD isoform appeared to be overexpressed. MDCK-MRP2 cell monolayers exhibited higher polarized efflux of vinblastine than Caco-2 and MDCK-WT cell monolayers. K(M) values for vinblastine in Caco-2 and MDCK-MRP2 cells were determined to be 71.8+/-11.6 and 137.3+/-33.6 microM. respectively, and Vmax values were determined to be (0.54+/-0.03 and 2.45+/-0.31 pmolcm(-2)s(-1), respectively. Known substrates/inhibitors of MRP2 showed differences in their ability to inhibit vinblastine efflux in Caco-2 cells as compared to MDCK-MRP2 cells CONCLUSIONS: These data suggest that MDCK-MRP2 cells overexpress only the 150 kD isoform of MRP2. The 190 kD isoform, which was also found in Caco-2 cells and MDCK-WT cells, was present in MDCK-MRP2 cells but not over expressed. The apparent kinetics constants and affinities of some MRP2 substrates were different in Caco-2 cells and MDCK-MRP2 cells. These differences in substrate activity could result from differences in the relative expression levels of the MRP2 isoforms present in Caco-2 cells and MDCK-MRP2 cells and/or differences in the partitioning of substrates in these two cell membrane bilayers.

Animals↗
PubMed2002

Are MDCK cells transfected with the human MDR1 gene a good model of the human intestinal mucosa?

PURPOSE: To investigate whether Madin-Darby canine kidney cells transfected with the human MDR1 gene (MDCK-MDR1) are a good model of the human intestinal mucosa. METHODS: P-glycoprotein (P-gp) expression in Caco-2 cells was compared with P-gp expression in MDCK wild- type (MDCK-WT) and MDCK-MDR1 cells using Western blotting methods. The polarized efflux activities of P-gp(s) in MDCK-MDRI cells, MDCK-WT cells, and Caco-2 cells were compared using digoxin as a substrate. Apparent Michaelis-Menten constants (K(M),Vmax) for the efflux of vinblastine in these three cell lines were determined. Apparent inhibition constants (K(I)) of known substrates/inhibitors of P-gp were determined by measuring their effects on the efflux of digoxin in Caco-2 or MDCK-MDR1 cell monolayers. RESULTS: MDCK-MDR1 cells expressed higher levels of P-gp compared to Caco-2 and MDCK-WT cells, as estimated by Western blots. Two isoforms of P-gp were expressed in Caco-2 and MDCK cells migrating with molecular weights of 150 kDa and 170 kDa. In MDCK-MDR1 cells, the 150 kDa isoforms appeared to be overexpressed. The MDCK-MDR1 cells exhibited higher polarized efflux of [3H]-digoxin than did Caco-2 and MDCK-WT cells. K(M) values of vinblastine in Caco-2. MDCK-WT, and MDCK-MDR1 cells were 89.2+/-26.1, 24.5+/-1.1, and 252.8+/-134.7 microM, respectively, whereas Vmax values were 1.77+/-0.22, 0.42+/-0.01, and 2.43+/-0.86 pmolcm(-2)s(-1), respectively. Known P-gp substrates/inhibitors showed, in general, lower K(I) values for inhibition of digoxin efflux in Caco-2 cells than in MDCK-MDR1 cells. CONCLUSIONS: These data suggest that the MDCK-MDR1 cells overexpress the 150 kDa isoform of P-gp. MDCK-MDR1 cells are a useful model for screening the P-gp substrate activity of drugs and drug candidates. However, the apparent kinetics constants and affinities of substrates determined in the MDCK-MDR1 cell model may be different than the values obtained in Caco-2 cells. These differences in substrate activity could result from differences in the relative expression levels of total P-gp in Caco-2 and MDCK-MDR1 cells and/or differences in the partitioning of substrates into these two cell membrane bilayers.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1990

Caco-2 cell monolayers as a model for drug transport across the intestinal mucosa.

Human colon adenocarcinoma (Caco-2) cells, when grown on semipermeable filters, spontaneously differentiate in culture to form confluent monolayers which both structurally and functionally resemble the small intestinal epithelium. Because of this property they show promise as a simple, in vitro model for the study of drug absorption and metabolism during absorption in the intestinal mucosa. In the present study, the transport of several model solutes across Caco-2 cell monolayers grown in the Transwell diffusion cell system was examined. Maximum transport rates were found for the actively transported substance glucose and the lipophilic solutes testosterone and salicyclic acid. Slower rates were observed for urea, hippurate, and saliylate anions and were correlated with the apparent partition coefficient of the solute. These results are similar to what is found with the same compounds in other, in vivo absorption model systems. It is concluded that the Caco-2 cell system may give useful predictions concerning the oral absorption potential of new drug substances.

Adenocarcinoma↗
PubMed1983

Changes of the activity and content of sucrase-isomaltase complex in the intestinal mucosa during the development of streptozotocin-induced diabetes in rats.

The changes in the activity and content of sucrase-isomaltase complex (S-I) in the intestinal mucosa were studied during the development of diabetes induced by streptozotocin in rats. On days 0, 1, 3, 5, and 10 after an intraperitoneal injection of streptozotocin (70 mg/kg), the enzyme activity and the enzyme content were observed in the jejunum and ileum. Sucrase and isomaltase activities markedly increased from the 3rd day both in the jejunum and ileum, and kept increasing till the 10th day especially in the ileum. The enzyme content of S-I also increased in parallel with its activity during the development of diabetes. However, in the early stage of diabetes, sucrase activity per microgram of S-I content increased both in the jejunum and ileum. Isomaltase activity per microgram of S-I content increased temporarily in the ileum. These results suggest that the increase of disaccharidase activities in the early stage of diabetes induced by streptozotocin is not only due to the increase of the enzyme content, but also due to the change of the enzyme catalytic property.

Animals↗
PubMed2005

The Vi capsular antigen of Salmonella enterica serotype Typhi reduces Toll-like receptor-dependent interleukin-8 expression in the intestinal mucosa.

Human infections with nontyphoidal Salmonella serotypes, such as S. enterica serotype Typhimurium, are characterized by a massive neutrophil influx in the colon and terminal ileum. In contrast, neutrophils are scarce in intestinal infiltrates of typhoid fever patients. Here, we show that in S. enterica serotype Typhi, the causative agent of typhoid fever, expression of the Vi capsular antigen reduced expression of the neutrophil chemoattractant interleukin-8 (IL-8) in host cells. Capsulated bacteria elicited IL-8 expression in polarized human epithelial cells (T84) and human macrophage-like cells (THP-1) in vitro at significantly reduced levels compared to noncapsulated bacteria. Experiments with a human cell line (HEK293) transfected with human Toll-like receptors (TLRs) demonstrated that in the presence of TLR5 or TLR4/MD2/CD14, a noncapsulated serotype Typhi mutant was able to induce the expression of IL-8, while this host response was significantly reduced when cells were infected with the capsulated serotype Typhi wild type. The relevance of these in vitro observations for the interaction of serotype Typhi with its human host was further studied ex vivo using human colonic tissue explants. Expression of IL-8 was detected in human colonic tissue explants infected with serotype Typhimurium or a noncapsulated serotype Typhi mutant. In contrast, infection with the serotype Typhi wild type did not elicit IL-8 expression in colonic tissue explants. Collectively, these data suggest that the scarcity of neutrophils in intestinal infiltrates of typhoid fever patients is due to a capsule-mediated reduction of TLR-dependent IL-8 production in the intestinal mucosa.

Antigens, Bacterial↗
PubMed2004

Apoptosis in the intestinal mucosa of patients with inflammatory bowel disease: evidence of altered expression of FasL and perforin cytotoxic pathways.

BACKGROUND AND AIMS: Abnormal apoptosis may result in the persistence of activated intestinal T-cells in inflammatory bowel disease (IBD). We investigated apoptosis in distinct mucosal compartments, and the expression of Fas/Fas ligand and perforin in the inflamed and non-inflamed intestinal mucosa of patients with IBD. METHODS: Colon specimens from 15 patients with ulcerative colitis (UC) and inflamed and non-inflamed mucosa from 15 patients with Crohn's disease (CD) were analysed for densities and distribution of apoptotic cells determined by the terminal deoxynucleotidyltransferase-mediated dUDP-biotin nick-end labelling (TUNEL) method. Fas, FasL, and perforin-expressing cells were assessed by immunoperoxidase, and with anti-CD3, anti-CD20 and anti-CD68, by double immunofluorescence with confocal microscopy. Quantitative analysis was performed using a computer-assisted image analyser. RESULTS: Colonic lamina propria (LP) and epithelium from patients with UC showed higher rates of apoptosis than controls, but no difference was shown regarding patients with CD. In LP, co-expression of Fas was reduced with T-cells in inflamed CD mucosa, and with macrophages in all patients with IBD. No difference was found in the expression of Fas on B-cells. Rates of FasL-expressing cells in LP were higher in IBD than in controls, with no correlation with the rates of apoptosis. Rates of perforin-expressing cells in LP were greater in UC than in controls, and correlated to the rates of apoptosis. No difference was shown regarding the inflamed and non-inflamed CD mucosa. Rates of FasL and perforin-expressing intra-epithelial lymphocytes showed no difference among groups. CONCLUSIONS: Increased expression of FasL in IBD colonic LP not parallelled by Fas on T-cells and macrophages may indicate a reduced susceptibility to the Fas/FasL-mediated apoptosis of lymphoid cells. Expression of perforin is correlated to the tissue damage, and may represent the enhancement of a distinct cytotoxic pathway in UC.

Adolescent↗
PubMed1983

Effects of feeding T-2 toxin on RNA, DNA and protein contents of liver and intestinal mucosa of rats.

Young male albino rats were fed 1.5 mg T-2 toxin/kg body weight daily for 4 days and the effects on body weight, liver weight and protein, RNA, and DNA contents of liver and intestinal mucosa were studied. A significant decrease in body weight and an increase in liver weight were observed. Liver protein and DNA and intestinal mucosal protein contents were significantly decreased, whereas intestinal mucosal RNA content was increased. Decreased liver and intestinal mucosal protein synthesis in T-2 toxin-fed rats was inferred from the [14C]leucine incorporation studies.

Animals↗
PubMed1972

A binding protein for fatty acids in cytosol of intestinal mucosa, liver, myocardium, and other tissues.

A protein of molecular weight approximately 12,000 which binds long-chain fatty acids and certain other lipids has been identified in cytosol of intestinal mucosa, liver, myocardium, adipose tissue, and kidney. Binding is noncovalent and is greater for unsaturated than for saturated and medium-chain fatty acids. This protein appears to be identical with the smaller of two previously described cytoplasmic anion-binding proteins. Binding of long-chain fatty acids by this protein is greater than that of other anions tested, including sulfobromophthalein, and does not depend on negative charge alone. The presence of this binding protein may explain previously observed differences in intestinal absorption among fatty acids, and the protein may participate in the utilization of long-chain fatty acids by many mammalian tissues.

Adipose Tissue↗