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PubMed1996

Differential expression of cysteine-rich intestinal protein in liver and intestine in CCl4-induced inflammation.

Cysteine-rich intestinal protein (CRIP) is a double zinc finger (LIM domain) protein that is developmentally regulated but has an unknown function. CRIP is highly expressed in the intestine, but expression is low in liver. To determine if CRIP expression is regulated under altered physiological status, we used CCl4-induced injury as a model to produce hepatic injury and systemic effects associated with inflammation. Since CRIP is a zinc finger protein and zinc decreases the hepatic response to CCl4, the effect of supplemental dietary zinc (300 mg/kg diet) was also examined. Our results show that this supplemental level of dietary zinc did not affect the index of hepatic injury (plasma alanine aminotransferase), indicating zinc did not have a protective effect. Liver CRIP mRNA increased with CCl4 and CRIP protein was shown by immunohistochemistry to be localized in hepatocytes near the vascular supply. In the intestine, CCl4 caused a transient decrease in CRIP mRNA, but supplemental dietary zinc treatment prevented this decrease. These current results show that CRIP expression changes in response to cellular damage due to acute hepatic injury and are consistent with a functional role for CRIP in proliferation, differentiation, or turnover.

Animals↗
PubMed1978

Development of digestive enzymes in the piglet from birth to 8 weeks. II. Intestine and intestinal disaccharidases.

The changes with age of intestinal mucosa, protein, lactase, maltase and sucrase were followed in the piglet between day 105 of gestation and 8 weeks after birth. Lactase and maltase activities appeared during fetal life in the whole of the small intestine. Activity of sucrase was recorded after the 1st postnatal week. Lactase activity was high at birth and reached a maximum at 1 week (X 2.5); maltase activity which was low at birth increased to the 8th week (X 143). Activities of all enzymes were low in the duodenum; lactase was most active in the jejumum. Similar activities of maltase and sucrase were found in the two distal parts of the small intestine. Specific activity (related to protein content) of lactase reached a maximum at the end of the 1st week after birth and decreased afterwards. Specific maltase and sucrase activities were higher in the 2nd week, decreased between the 2nd and 4th week and increased afterwards (maltase) or decreased to the 6th--8th week (sucrase).

Age Factors↗
PubMed1987

Rise of prostanoids in rat small intestinal mucosa following intestinal protein hypersensitivity.

The purpose of the present study was to establish whether there is an elevated prostaglandin concentration in the intestinal mucosa in rats suffering from an immediate type hypersensitivity reaction. Rats of the Hooded-Lister strain were sensitized and challenged with ovalbumin. Control rats were given adjuvant only. Prostanoid content of scraped mucosa was determined by radioimmunoassay. It was found that the prostaglandin E2 content in the sensitized intestine was significantly elevated as compared to the controls. There was no significant rise of 6-keto prostaglandin F alpha or thromboxane E2 in the sensitized rats. These results show that prostaglandin B2 participates in intestinal immediate type responses and may explain some of the clinical manifestations of food protein allergy.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Intestinal mucosa of celiacs in remission is unable to abolish toxicity of gliadin peptides on in vitro developing fetal rat intestine and cultured atrophic celiac mucosa.

Subfraction 2R of fraction 9 from a peptic-tryptic-pancreatic digest of wheat gliadin is known to be toxic in vivo to celiac patients. We have found that fractions 9 and 2R inhibit the in vitro development of fetal rat intestine and the increase of enterocyte height occurring in organ culture of atrophic celiac mucosa (0.1-0.5 mg/ml medium). Other peptide fractions of the gliadin digest are devoid of such in vitro effects. Subfraction 2R, after incubation with morphologically normal small intestinal mucosa of celiacs in remission and ultrafiltration, was still very active in both culture systems at low concentration (0.1 mg/ml); on the contrary, subfraction 2R was inactivated after incubation with normal mucosa. These results are compatible with the hypothesis that there is a mucosal defect in handling gliadin peptides in celiac disease, and suggest that there is either a primary (or secondary) enzyme deficiency or some other mechanism operating in the intestinal mucosa of celiac patients in remission.

Animals↗
PubMed1995

Intestinal absorption of azetirelin, a new thyrotropin-releasing hormone (TRH) analogue. II. In situ and in vitro absorption characteristics of azetirelin from the rat intestine.

Intestinal absorption characteristics of azetirelin, a new thyrotropin-releasing hormone (TRH) analogue, were studied in rats by means of in situ closed loop and in vitro everted sac experiments. Plasma concentrations of azetirelin obtained in the in situ closed loop experiments were not significantly different among the intestinal segments. Area under the plasma concentration-time curve (AUC) of azetirelin following administration into the duodenal loop increased in proportion to the dose. The serosal to mucosal concentration ratio of the analogue in the everted sac experiment was constant over the mucosal drug concentration range of 0.01-10 mM. There was no directional difference in the transfer rate of azetirelin across the everted and non-everted sacs of the duodenum. Furthermore, its transport across the duodenum was not influenced by low incubation temperature (25 degrees C), addition of dipeptide (Gly-Gly), or pretreatment of the mucosal surface with 2,4-dinitrophenol, while that of TRH was inhibited under these conditions. These results suggest that the intestinal absorption mechanism of azetirelin is different from that of TRH, and that azetirelin is predominantly transported via a passive diffusion.

Amino Acid Sequence↗
PubMed1976

Megacystis-microcolon-intestinal hypoperistalsis syndrome: a new cause of intestinal obstruction in the newborn. Report of radiologic findings in five newborn girls.

Five newborn girls presented with small intestinal obstruction and microcolon and a giant bladder (megacystis). Organic causes of obstruction were not found, and the gastrointestinal tract failed to function after appropriate diversion. Two died in the postoperative period, two lived several months on central venous hyperalimentation, and one died at 34 months of age following chronic though intermittent hyperalimentation. Pathologic studies showed an abundance of ganglion cells in both dilated and narrowed areas of intestine; the combined small bowel-colon length was one-third of normal in the absence of an evident obstructive or vascular insult. The five patients represent the most severe manifestation of defective intestinal peristalsis in a larger group of distended newborns in whom organic gastrointestinal obstruction is not found. Treatment with central venous hyperalimentation may sustain life, and some patients eventually recover gastrointestinal function. The hypoperistalsis is largely refractory to pharmacologic treatment; its cause is unknown.

Abnormalities, Multiple↗
PubMed1981

Effect of dietary corn starch intake on ruminal, small intestinal and large intestinal starch digestion in cattle.

In Exp. 1, 24 yearling Holstein steers averaging 340 kg were fed either an alfalfa hay diet at a maintenance level of metabolizable energy (ME) intake or corn silage-corn diets at one, two or three times maintenance ME intake. After a 42-day adjustment period, steers were fed individually, and digestibilities of total alpha-glucosides, starch oligosaccharides and glucose were determined at 2-week intervals, with chromic oxide used as an indicator. Steers fed the alfalfa hay diet had higher (P less than .05) total tract digestibilities of total alpha-glucosides and starch than steers fed the corn diets. Fecal starch (percentage of dry matter) in steers fed the corn diets increased (P less than .05) from approximately 11 to 31% as level of ME intake increased from one to three times maintenance. Starch digestibilities for the corn diets fed at one, two and three times maintenance were 81.4, 76.4 and 76.0%, respectively. However, these trends toward reduced starch digestibilities were not significant. There appeared to be no apparent adaption of alpha-glucoside digestibility in the total digestive tract among steers fed different levels of corn over the intervals observed. In Exp. 2, four Holstein steers (350 KH) were each fitted with duodenal and ileal reentrant cannulas and fed either a low or a high level of corn. Alpha-glucoside intakes for animals given the low and high levels of cord averaged 1.7 and 3.2 kg, respectively. Steers fed the high level of corn digested more (p less than .05) alpha-glucoside in the total tract (2.9 vs 1.6 kg), reticulo-rumen (2.3 vs 1.2 kg) and large intestine level of corn. Steers fed the high level of corn also digested more corn in the small intestine (.415 vs .221 kg) than steers fed the lower level; however, differences were not significant. Although there were trends toward lower partial digestion coefficients (expressed as a percentage of alpha-glucoside presented to that segment) in the total tract, reticulo-rumen and small intestine for steers fed the high corn diet, the magnitude of the differences was not significant.

Animals↗
PubMed1981

Intestinal absorption of D-galactose and L-leucine and intestinal disaccharidase activities in growing chickens fed different raw legume diets.

A significant (P less than .01) impairment in the rate of growth, along with a significant (P less than .01) inhibition in the rate of in vivo intestinal absorption of D-galactose and L-leucine, and in the in vitro intestinal absorption of D-galactose, was found in growing chickens fed ad libitum over a 60-day period, diets containing the raw legumes Vicia faba, Glycine soja, Vicia ervilia, and Phaseolus vulgaris as the main source of protein. Furthermore, a significant (P less than .01) reduction in the intestinal disaccharidase activity was found in the legume-fed chickens. The possible nature of these effects was discussed.

Animal Feed↗
PubMed2001

Spontaneous and continuous cyclooxygenase-2-dependent prostaglandin E2 production by stromal cells in the murine small intestine lamina propria: directing the tone of the intestinal immune response.

The mechanisms allowing the gastrointestinal immune system to avoid an inappropriate inflammatory response to nonpathogenic luminal Ags are poorly understood. We have previously described a role for cyclooxygenase (COX)-2-dependent arachidonic acid metabolites produced by the murine small intestine lamina propria in controlling the immune response to a dietary Ag. To better understand the role of COX-2-dependent arachidonic acid metabolites produced by the lamina propria, we examined the pattern of expression and the cellular source of COX-2 and COX-2-dependent PGE(2). We now demonstrate that non-bone marrow-derived lamina propria stromal cells have basal COX-2 expression and that COX-2-dependent PGE(2) production by these cells is spontaneous and continuous. The other mucosal and nonmucosal lymphoid compartments examined do not share this phenotype. In contrast to the majority of descriptions of COX-2 expression, COX-2 expression by lamina propria stromal cells is not dependent upon exogenous stimuli, including adhesion, LPS signaling via Toll-like receptor 4, or the proinflammatory cytokines TNF-alpha, IFN-gamma, and IL-1 beta. These findings, in conjunction with the known immunomodulatory capacities of PGs, suggest that COX-2 expression by the small intestine lamina propria is a basal state contributing to the hyporesponsiveness of the intestinal immune response.

Animals↗
PubMed2005

The characterization of intraepithelial lymphocytes, lamina propria leukocytes, and isolated lymphoid follicles in the large intestine of mice infected with the intestinal nematode parasite Trichuris muris.

Despite a growing understanding of the role of cytokines in immunity to the parasitic helminth Trichuris muris, the local effector mechanism culminating in the expulsion of worms from the large intestine is not known. We used flow cytometry and immunohistochemistry to characterize the phenotype of large intestinal intraepithelial lymphocytes (IEL) and lamina propria leukocytes (LPL) from resistant and susceptible strains of mouse infected with T. muris. Leukocytes accumulated in the epithelium and lamina propria after infection, revealing marked differences between the different strains of mouse. In resistant mice, which mount a Th2 response, the number of infiltrating CD4+, CD8+, B220+, and F4/80+ IEL and LPL was generally highest around the time of worm expulsion from the gut, at which point the inflammation was dominated by CD4+ IEL and F4/80+ LPL. In contrast, in susceptible mice, which mount a Th1 response, the number of IEL and LPL increased more gradually and was highest after a chronic infection had developed. At this point, CD8+ IEL and F4/80+ LPL were predominant. Therefore, this study reveals the local immune responses underlying the expulsion of worms or the persistence of a chronic infection in resistant and susceptible strains of mouse, respectively. In addition, for the first time, we illustrate isolated lymphoid follicles in the large intestine, consisting of B cells interspersed with CD4+ T cells and having a central zone of rapidly proliferating cells. Furthermore, we demonstrate the organogenesis of these structures in response to T. muris infection.

Animals↗
PubMedDate not supplied

[The immuno-microbiological characteristics of the small intestine and the translocation of the enteral microflora in acute intestinal obstruction].

The complex examination of 72 patients with acute ileus (AI) of nontumor nature with different severity of endotoxicosis was carried out. The study revealed that AI was accompanied by deep suppression of the immunosecretory and motor evacuatory function of the small intestine, as well as by its pronounced bacterial contamination, mainly due to the significant quantitative prevalence of Gram-negative microflora. The combination of these factors played the key role in the increase of the permeability of the enteric barrier for symbiotic microflora and its massive translocation from the intestinal tract to the internal organs of the body (peritoneal exudate, portal bed), which directly correlated with the severity of endotoxicosis in AI patients. The deficiency of the barrier function of the liver was accompanied by the penetration of infective agents into the general blood stream, thus causing the development of endotoxic shock in AI patients. The analysis of the results thus obtained made it possible to determine the main ways for the elimination of intestinogenic intoxication in AI; they should be aimed at the bacterial decontamination of the small intestine, the restoration of its motor evacuatory and protective barrier functions, the liquidation of portal and systemic bacteremia, the correction of the functional deficiency of the liver.

Acute Disease↗
PubMed2001

Modulation of intestinal permeability by nitric oxide donors: implications in intestinal delivery of poorly absorbable drugs.

The effects of nitric oxide (NO) donors NOC5 [3-(2-hydroxy-1-(methylethyl)-2-nitrosohydrazino)-1-propanamine ] and NOC12 [N-ethyl-2-(1-ethyl-hydroxy-2-nitrosohydrazino)-ethanamine] on the permeability of 5(6)-carboxyfluorescein (CF) across the intestinal membrane were examined by an in vitro Ussing chamber method. The NO donors significantly increased the intestinal permeability of CF and their absorption-enhancing effects were concentration-dependent over the range of 0.01 to 0.1 mM. Regional differences in the absorption-enhancing effects of the NO donors were observed (colon > jejunum). The absorption-enhancing effect of NOC12 reduced as the molecular weights of compounds increased. Therefore, the degree of absorption-enhancing effect of NOC12 was dependent on the molecular weights of compounds. In the pretreatment studies with NOC12 and lactate dehydrogenase release studies, the absorption-enhancing effect of 0.1 mM NOC12 was reversible and less toxic to the colonic membrane. On the other hand, the absorption-enhancing effect of NOC12 was inhibited by the coadministration of 2-(4-carboxyphenyl) 4,4,5, 5-tetramethylimidazole-1-oxyl 3-oxide sodium salt, an NO scavenger, suggesting that NO can regulate the permeability of water-soluble drugs in the gut. Furthermore, NOC12 (0.1 and 1 mM) significantly decreased the transepithelial electrical resistance value of the colonic membrane, suggesting that the absorption-enhancing mechanism of NOC12 may be partly related to the dilation of the tight junction in the epithelium via a paracellular route. These findings suggest that NO donors may be useful to enhance the intestinal absorption of poorly absorbable drugs.

Animals↗
PubMed1975

Thiamine absorption in the rat. ii. intestinal alkaline phosphatase activity and thiamine absorption from rat small intestine in-vitro and in-vivo.

The correlations between intestinal alkaline phosphatase (IAP) activity and thiamine absorption and glucose absorption were studied in the rat. An everted sac in-vitro technique was used in adult rats whereas in-vitro experiments were performed in young rats 10 days old. All incubation experiments were done with 14-C-labeled thiamine. The patterns of IAP activity along the small intestines differed greatly between young and adult rats but were closely paralleled by the distribution of active thiamine transport in adult rats and thiamine absorption in young rats, respectively. When IAP was specifically inhibited in adult rats by L-phenylalanine active thiamine transport in-vitro was abolished. No correlation was found between IAP activity and active transport or glucose in-vitro, nor did inhibition of the enzyme in any way affect glucose transport capacity. It is suggested that the enzyme intestinal alkalinephosphatase is involved in the process of active thiamine absorption.

Age Factors↗
PubMedDate not supplied

[Populational alteration of cells in the intestinal intraepithelial layer and morphological changes of the intestinal wall elicited by Toxocara vitulorum infection in buffalo calves (Bubalus bubalis)].

To understand the development of the inflammatory responses in the wall of the gut, during the process of expulsion of the parasites from the host, samples of tissues were removed from the small intestines from four groups of naturally infected buffalo calves with Toxocara vitulorum during the beginning of the infection, at the peak of egg output, during the period of expulsion and post-expulsion of the worms, as well as from uninfected calves. Cells (mast cells, eosinophils, intraepithelial lymphocytes - IEL and goblet cells) present in the epithelial layer (intraepithelial) of the small intestine were counted. In the duodenum, jejunum and ileum, the population of mast cells, eosinophils and lymphocytes increased significantly during the peak of the infection. Goblet cell numbers increased also during the beginning and at the peak of the infection. The decline of the number of these cells occurred during the periods of expulsion of the worms reaching to uninfected control counts at the post-expulsion period indicating a role of these cells in the process of expulsion of T. vitulorum by the buffalo calves. The layers of the intestinal wall (villus, crypt, submucosa and muscular) were also measured. Morphological examinations showed a significant vilar atrophy, particularly in the duodenum during the beginning, peak and during the period of expulsion of the worms, but smooth muscle hypertrophy or other alteration was not observed in any period of the infection.

Animals↗
PubMed1991

Identification and characterization of rat intestinal keratins. Molecular cloning of cDNAs encoding cytokeratins 8, 19, and a new 49-kDa type I cytokeratin (cytokeratin 21) expressed by differentiated intestinal epithelial cells.

In the previous paper (Quaroni, A., Calnek, D., Quaroni, E., and Chandler, J.S. (1991) J. Biol. Chem. 266, 11923-11931) we describe the use of a panel of "antikeratin" monoclonal antibodies to study cytokeratin distribution in rat intestinal epithelium. In the present paper we describe the use of three antikeratin monoclonal antibodies to identify and recovery cDNA clones expressing immunologically specific fusion proteins from a rat intestinal cDNA library. DNA sequence analysis identified each cDNA encoded epitope including the carboxyl-terminal portions of cytokeratins 8 and 19 (as cataloged by Moll, R., Franke, W.W., and Schiller, D.L. (1982) Cell 31, 11-24) recognized by antibodies RK4 and RK7, respectively. In addition, antibody RK5 was used to recover a cDNA clone (pRK5) encoding a portion of a 48-kDa keratin-related protein with unique tissue and cellular distribution, designated cytokeratin 21. Translation of cDNA-selected mRNAs yielded individual proteins which could be resolved and identified by their specific immunoreactivities. The pRK5 cDNA was used to recover a larger (approximately 1.3 kilobase pairs) cDNA clone (KB2) from an independent cDNA library for DNA sequence analysis and for the recovery of additional overlapping cDNA clones. The resulting cDNA sequence (1519 base pairs) contains the complete coding region of cytokeratin 21 (49,387 daltons). The predicted amino acid sequence of cytokeratin 21 confirms its identity as a novel type I cytokeratin expressed predominantly in the intestinal epithelium.

Amino Acid Sequence↗
PubMed1990

[Naso-intestinal endoscopic intubation in the complex treatment of postoperative intestinal obstruction].

The long-tube decompression was used for treatment of 54 selected patients with diagnosis of early postoperative intestinal obstruction. For this purpose a silicon double-lumen wire-guided tube has been endoscopically introduced into the proximal portion of the small intestine. In 40 cases continuous decompression of the small bowel brought about a successful resolution of intestinal obstruction by nonoperative therapy. Failure of the conservative treatment within the first 48 hours after intubation has led to operation in 14 cases. Six patients died in this series (4 patients died of multiple organ failure, 2--of thromboembolism). The study has shown that the method can be successfully used.

Abdomen, Acute↗
PubMed1990

[Behavior of pO2 on rabbit small intestine serosa, measured with the Clark electrode in different models of intestinal ischemia].

The pO2 on the surface of the small intestine serosa was measured on an isolated small intestine loop of the rabbit after synchronistic arterial and venous ligature of the mesenterium, after synchronistic arterial starvation and venous ligature, and after torsion of the mesenterium. The measurements of the pO2 were carried out by means of a Clark-electrode. Different periods for the decrease of the pO2 to zero Torr were shown in the different models of intestinal ischemia. Only the difference between the synchronistic arterial and venous ligature and torsion was statistically significant.

Animals↗
PubMed1989

Intestinal lymphangiomas: a rare cause of intestinal obstruction.

Intestinal obstruction developed in a 4-month-old child in association with an ileal lymphangioma. Intestinal lymphangiomas have only rarely been reported in the literature. This case report documents an additional case and also points out an association with intestinal obstruction. The clinical and pathologic details of lymphangiomas are also reviewed.

Female↗