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At least 613 records · Page 34Linked to original sources
PubMed1988

Leucine and the intestinal phase of gastric acid secretion.

The intestinal phase of gastric acid secretion is mediated by the putative hormone entero-oxyntin. The release of the hormone has been demonstrated in both dog and rat models during an intestinal meal of liver extract. The maximal gastric acid response to pentagastrin is augmented by the presence of liver extract in the intestine; this phenomenon serves as a bioassay for entero-oxyntin. We tested the hypothesis that one or more amino acids in liver extract causes the release and/or action of entero-oxyntin. Anesthetized rats, prepared with bilateral cervical vagotomies, received jejunal perfusion of mannitol (control), liver extract, or an amino acid. Intravenous pentagastrin was administered simultaneously at a dose known to produce maximal gastric acid output in rats. Our results show that of the amino acids tested, only leucine produced a significant augmentation of maximal pentagastrin-stimulated gastric acid secretion when compared with controls.

Amino Acids↗
PubMed1996

Relationship of phosphatidylcholine to hydrophobic surfactant on rat intestinal chylomicron secretion.

Hydrophobic surfactants such as Poloxalene inhibit triglyceride secretion into lymph by enterocytes. The inhibitory effect of these agents on triglyceride secretion is reversed when lipid presented for absorption is exclusively in the form of phosphatidylcholine (PC) and not triglyceride. The present investigation performed in conscious mesenteric lymph fistula rats was designed to determine whether various mixtures of triglyceride and PC given intraduodenally with Poloxalene would also reverse the inhibitory effect of Poloxalene on triglyceride secretion into lymph. A 50-50 mixture of triolein (TO) and PC resulted in normal triglyceride secretion into lymph. However, when the mixture of lipids was 75-25, TO to PC, results for triglyceride recovery in lymph were considerably reduced. The transport rate for triglyceride into lymph was not as depressed, however, as observed for Poloxalene treated rats given lipid for absorption basically in the triglyceride form. Substitution of phosphatidylethanolamine for PC had no beneficial effect on triglyceride secretion in Poloxalene treated rats. It is concluded that PC can reverse the inhibitory effect of Poloxalene on triglyceride secretion into lymph even when considerable amounts of triglyceride along with PC are presented for absorption.

Animals↗
PubMed2006

Caspase and bid involvement in Clostridium difficile toxin A-induced apoptosis and modulation of toxin A effects by glutamine and alanyl-glutamine in vivo and in vitro.

Clostridium difficile is the leading cause of nosocomial bacterial diarrhea. Glutamine and its stable and highly soluble derivative alanyl-glutamine, have been beneficial in models of intestinal injury. In this study, we extend our work on the mechanisms of Clostridium difficile toxin A (TxA)-induced apoptosis in human intestinal epithelial T84 cells and evaluate the effects of glutamine and alanyl-glutamine on TxA-induced apoptosis in vitro and disruption of ileal mucosa in vivo. T84 cells were incubated with TxA (100 ng/ml) in medium with or without glutamine or alanyl-glutamine (3 to 100 mM). Apoptosis was evaluated by DNA fragmentation in vitro and the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling method in vivo. Caspase and Bid involvement were investigated by Western blotting. Ligated rabbit ileal loops were used for the evaluation of intestinal secretion, mucosal disruption, and apoptosis. TxA induced caspases 6, 8, and 9 prior to caspase 3 activation in T84 cells and induced Bid cleavage by a caspase-independent mechanism. Glutamine or alanyl-glutamine significantly reduced TxA-induced apoptosis of T84 cells by 47% and inhibited activation of caspase 8. Both glutamine and alanyl-glutamine reduced TxA-induced ileal mucosal disruption and secretion. Altogether, we further delineated the apoptosis-signaling cascade induced by TxA in T84 cells and demonstrated the protective effects of glutamine and alanyl-glutamine. Glutamine and alanyl-glutamine inhibited the apoptosis of T84 cells by preventing caspase 8 activation and reduced TxA-induced intestinal secretion and disruption.

Animals↗
PubMed1992

Immunological characterization of a 17-kDa antigen from Cryptosporidium parvum recognized early by mucosal IgA antibodies.

Cryptosporidium parvum antigens were characterized by immunoblot analysis of sera and intestinal secretions of BALB/c mice orally infected with 10(5) oocysts. A major band at 17 kDa under non-reduced conditions and at 18 kDa under reduced conditions was recognized by anti-C. parvum IgA and IgG in serum and intestinal secretions from day 15 post-infection. This recognition persisted throughout the experiment (day 30). Mouse-serum antibodies raised against the 17-kDa purified antigen (P17) showed no cross-reactivity with other C. parvum antigens. Immunofluorescence study revealed that this antigen is located on the sporozoite. It is suggested that this antigen could be a good candidate for studies of mucosal immune response to C. parvum and for vaccination.

Animals↗
PubMed1981

Nicotinic acid inhibits enterotoxin-induced jejunal secretion in the pig.

The use of nicotinic acid for preventing intestinal secretion caused by cholera toxin and by the heat-stable enterotoxin of Escherichia coli has been investigated in the weanling pig. Secretory effects were measured in ligated jejunal loops of halothane-anesthetized pigs by dilution of a nonabsorbable marker added to the loop fluid. Different routes of administration and different initial pH values for nicotinate solutions were studied to determine optimal conditions for secretory inhibition. The neutral sodium salt of nicotinic acid had no significant antisecretory activity under any conditions used in these trials. Inhibition of secretion was most effective with partly neutralized nicotinic acid at pH 4.5 added directly to loops containing enterotoxin. Net fluid secretion induced by cholera toxin or heat-stable enterotoxin of E. coli was prevented by this treatment. Reversal of secretion was not accompanied by any measurable changes in cyclic nucleotide concentration in intestinal mucosa. Nicotinic acid antagonism of a secretory step common to cholera toxin and heat-stable enterotoxin of E. coli but subsequent to cyclic nucleotide involvement is indicated by these data.

Animals↗
PubMed1995

Substance P induces ion secretion in mouse small intestine through effects on enteric nerves and mast cells.

We used genetically mast cell-deficient WBB6F1 W/Wv (W/Wv) mice and congenic WBB6F1 +/+ normal (+/+) mice to examine the role of mast cells in substance P-induced intestinal ion secretion. Isolated sheets prepared from segments of the midportion of the small intestine were studied in Ussing chambers. Substance P caused a dose-dependent increase in short-circuit current (Isc) that was approximately 50% less in intestine from W/Wv than from +/+ mice. Similar results were obtained for substance P-(4-11) (the COOH terminus) and substance P methyl ester [a selective neurokinin (NK)-1 agonist]. Histamine H1 or H2 antagonists reduced the Isc responses to substance P in intestine from +/+ mice but had no effect in intestine from W/Wv mice. In addition, reconstitution of intestinal mast cells in W/Wv mice by intravenous injection of +/+ bone marrow cells normalized the tissues' secretory responses to substance P or substance P methyl ester. However, in W/Wv and +/+ mice, the selective NK1 antagonist CP-96345 virtually abolished intestinal responses to substance P, and the responses were also markedly inhibited by neural blockade with tetrodotoxin. In contrast, in tetrodotoxin-pretreated intestine, histamine antagonism caused a further reduction in the responses to substance P only in +/+ mouse tissues. Taken together, our results suggest that the effects of substance P on intestinal Isc KN1 receptors but that the neuropeptide acts via effects on enteric nerves and mast cells. The data thus support the concept that mast cells and enteric nerves participate in the regulation of substance P-induced intestinal ion secretion.

Animals↗
PubMed1997

Rapid synthesis and secretion of intestinal apolipoprotein A-IV after gastric fat loading in rats.

To further investigate the possible role of apolipoprotein A-IV (apo A-IV) in the short-term control of food intake, we examined the kinetics of intestinal apo A-IV synthesis and release into lymph and plasma after intragastric delivery of physiological amounts of lipid. Within 30 min of intragastric administration of 0.1 g of triglyceride, plasma and lymph levels of apo A-IV were similar to those produced by exogenous apo A-IV that inhibit food intake. Within 15 min, 5% of gastrically delivered radioactive lipid reached the distal small bowel and cecum; by 30 min radioactivity was evenly distributed throughout the small intestine, with 10-15% of the load in the distal gut. By 30 min, synthesis of apo A-IV was significantly stimulated in proximal and distal jejunum and distal ileum and remained elevated up to 4 h after the delivery of lipid. Our results indicate that the delivery of physiological amounts of lipid into the stomach produces a significant and rapid stimulation of apo A-IV secretion into lymph and plasma, together with a rapid delivery of lipid and increases in mucosal synthesis of apo A-IV along the entire length of the small intestine. The results support a possible role for apo A-IV in the short-term control of food intake and suggest a role for the entire gut in the integrative response of apo A-IV to a fat meal.

Animals↗
PubMed1983

Effect of acid secretory capacity and chronic endogenous hypergastrinemia on pancreatic secretion and intestinal morphology in the rat.

To study the trophic effects of gastrin on the gastrointestinal tract, chronic endogenous hypergastrinemia was produced in rats by implantation of the gastric antrum into the colon. Rats were sham-operated (normal gastrin, normal acid) or were prepared with BII gastrojejunostomy and antral resection (low gastrin, low acid), or BII gastrojejunostomy and antral implantation into colon (high gastrin, acid present). To separate effects of hypergastrinemia from those of acid hypersecretion, two additional groups were prepared with total gastrectomy and either resection of the antrum (low gastrin, no acid) or antral implantation into colon (high gastrin, no acid). After 12 weeks, the pancreatic secretory response to secretin was measured. The animals were then sacrificed, and liver, pancreas, small intestine, and colon were weighed. In separate groups of animals villous height and width and crypt depth of small intestine and transverse colon were measured. Serum gastrin concentrations increased three- to fivefold in fasting and fed antral implant animals. Serum gastrin levels in the fed state were lower in antrectomy rats compared to controls but did not differ in the fasting rats. Pancreas and colon were heavier in all hypergastrinemic rats. Liver weights did not differ between hypergastrinemic animals and controls. Stimulated pancreatic bicarbonate secretion following secretin infusion was elevated only in hypergastrinemic, hyperacidic rats. Hypertrophy of the small bowel was seen in antral implant rats only when the gastric remnant was preserved (ie, when acid was present). Colonic mucosal thickness was increased in antral implant rats with or without gastrectomy. No significant increases in small-bowel villous height or crypt depth were found in antral implant rats. Thus, chronic endogenous hypergastrinemia caused pancreatic and colonic hypertrophy independent of acid secretion. In addition to hypergastrinemia, gastric hyperacidity was also needed for enlargement of small bowel or increase in secretin-stimulated pancreatic bicarbonate secretion.

Animals↗
PubMedDate not supplied

Purification and identification of turkey immunoglobulin-A.

Turkey immunoglobulin-A (IgA) was isolated from bile, intestinal secretions, and serum by affinity chromatography using monospecific anti-turkey IgA coupled to CNBr-activated Sepharose. The isolated immunoglobulin was antigenically distinct from IgM and IgG. The purity of IgA was demonstrated by immunodiffusion, immunoelectrophoresis, and analytical ultracentrifugation. The predominant forms of polymeric IgA in bile and intestinal secretions had respective So20w values of 16.1 and 15.2. Larger polymers (25-26S) were also present. Two molecular forms (8.5S and 17S) were found in serum. The 8.5S peak was higher than the 17S, indicating a greater concentration of 8.5 S.

Animals↗
PubMed1988

Combined parenteral and oral immunization results in an enhanced mucosal immunoglobulin A response to Shigella flexneri.

Achieving a vigorous secretory immunoglobulin A (IgA) response in intestinal secretions usually requires multiple doses of antigen given orally, while systemic immunity is more easily attained by parenteral immunization. This study examines the role of combined parenteral and oral immunizations to enhance the early mucosal immune response to an enteropathogen. We have used a chronically isolated intestinal-loop model in rabbits as a probe to monitor kinetically the initial (primary) local immune response to shigella lipopolysaccharide (LPS) following combinations of parenteral immunization intramuscularly (i.m.) and oral stimulation with shigellae. Predictably, effective stimulation of systemic immunity was elicited when heat-killed preparations of Shigella sp. strain X16 were given i.m., as shown by strong serum IgG and weak intestinal IgA activity to shigella LPS. A single oral dose of live Shigella sp. strain X16 given to unprimed rabbits elicited only a typical weak IgA response in intestinal secretions. However, when an i.m. dose of heat-killed shigellae was followed 1 day later by an oral dose of live Shigella sp. strain X16, a hyperstimulation of the early secretory IgA response was elicited, and the response reached levels found previously only after multiple oral administrations of live shigellae. This stimulation did not require the use of an adjuvant. At the same time, the animals receiving this combined oral and i.m. regimen had a lower IgG antishigella LPS activity in serum compared with their response after receiving parenteral antigen in adjuvant alone. These findings indicate that while a dichotomy exists between the systemic and mucosal immune responses, careful orchestration of the stimulatory events can promote a vigorous early local IgA response.

Adjuvants, Immunologic↗
PubMed2003

Antibody responses in the serum and gut of chicken lines differing in cecal carriage of Salmonella enteritidis.

Salmonella frequently causes human foodborne infections. Contaminated products from poultry infected with Salmonella enteritidis are mainly involved. This serovar is able to colonize the gastrointestinal tract and generally produces a chronic asymptomatic carrier state in poultry, except in very young birds. We have developed a model of S. enteritidis carriage in chicks and found that four chicken lines, B13, L2, PA12 and Y11 differ in their cecal colonization by S. enteritidis, whereas their systemic organs are similarly infected. We have monitored the serum and gut antibody responses of these four lines to S. enteritidis for 9 weeks post inoculation (pi). We confirm that S. enteritidis infected the spleens of the four chicken lines similarly, and that it often colonized the ceca at levels significantly higher in B13 and L2 chicks than those of the PA12 and Y11 chicks. The serum IgM and IgG antibody responses were high and the serum IgA antibody responses low. In contrast, the intestinal secretions contained mostly IgA antibodies. The serum IgM antibody values of the four chicken lines were similar. However, the B13 and L2 chicks often had significantly higher serum IgG and IgA antibody responses than PA12 and Y11 chicks. Only the B13 and L2 chicks showed high, persistent levels of IgA antibody in intestinal secretions. These results suggest that most antibody responses are related to cecal colonization by S. enteritidis. They also indicate that factors other than the antibody levels are involved in the control of this colonization.

Animals↗
PubMed1999

Butyrate switches the pattern of chemokine secretion by intestinal epithelial cells through histone acetylation.

BACKGROUND: Butyrate, a fermentation product of intestinal bacteria, modifies chromatin structure through histone acetylation, thereby altering gene transcription. IL-8 and MCP-1 are chemokines, expressed by intestinal epithelial cells, which attract neutrophils and monocytes, respectively. We hypothesized that butyrate may alter IL-8 and MCP-1 expression by intestinal epithelial cells through histone acetylation. MATERIALS AND METHODS: IL-8 and MCP-1 expression was measured by ELISA and RNA transfer blots. Acetylated histones were separated on acetic acid-urea-triton gels. Butyrate was compared to Trichostatin-A, a specific inhibitor of histone deacetylase and to other short chain fatty acids. RESULTS: Caco-2 cells constitutively secreted MCP-1 but not IL-8. Butyrate reversibly decreased MCP-1 secretion. In contrast, butyrate increased IL-8 production. The effects of butyrate and Trichostatin-A were greater when cells were stimulated with IL-1beta. Butyrate and Trichostatin-A both increased histone acetylation. Trichostatin-A and other short chain fatty acids altered chemokine secretion according to their effect on histone acetylation. CONCLUSIONS: Butyrate reversibly switches chemokine secretion by epithelial cells through histone acetylation. We speculate that butyrate carries information from resident bacteria to epithelial cells. Epithelial cells transduce this signal through histone acetylation, modulating the secretion of chemokines.

Acetylation↗
PubMed1998

The effects of bacterial overgrowth and hemorrhagic shock on mucosal immunity.

Impairment in systemic and mucosal immune function is noted after hemorrhagic shock (HS). Overgrowth of gut microflora is common after shock insults and may act as a reservoir for intensive care unit-acquired infections and subsequent remote organ failure. Secretory immunoglobulin A (IgA), the principle immunoglobulin in intestinal secretions, is the first line of defense of mucosal surfaces. Although HS and gut bacterial overgrowth are often temporarily related, their combined effect on IgA is unknown and served as the basis for this study. After sham or HS, self-filling blind loops (SFBL) were created to affect bacterial overgrowth. Intestinal secretions were obtained 7 days later from SFBL and jejunal segments for quantitative culture. Gut washings were also obtained and secretory IgA levels determined by enzyme-linked immunosorbent assay. Bacterial overgrowth in the SFBL was associated with significant increases in IgA levels in the sham group only. IgA levels were depressed in both jejunal and SFBL segments in the HS group. Impaired humoral mucosal defense may be important mechanistically in the development of nosocomial infections and organ failure after HS, particularly with concurrent gut bacterial overgrowth.

Animals↗
PubMed2003

Leptin mediates Clostridium difficile toxin A-induced enteritis in mice.

BACKGROUND & AIMS: Leptin regulates energy homeostasis and participates in the regulation of the hypothalamic-pituitary-adrenal axis. Although hyperleptinemia is described in experimental colitis, its role in the pathophysiology of enterotoxin-mediated diarrhea and inflammation remains unclear. We examined the role of leptin in the inflammatory diarrhea induced by toxin A from Clostridium difficile, the causative agent of antibiotic-related colitis. METHODS: Toxin A (10 microg) or buffer were administered in ileal loops of leptin-deficient (ob/ob), leptin-resistant (db/db), or wild-type mice and enterotoxic responses were measured. RESULTS: In toxin A-treated wild-type mice, circulating leptin and corticosterone levels were increased compared with buffer-injected animals. Toxin A also stimulated increased mucosal expression of the Ob-Rb at the messenger RNA (mRNA) and protein level. Ob/ob and db/db mice were partially protected against toxin A-induced intestinal secretion and inflammation, and this effect was reversed by leptin administration in ob/ob, but not db/db, mice. Basal- and toxin A-stimulated plasma corticosterone levels in ob/ob and db/db mice were higher compared with toxin A-treated wild-type mice. To assess whether the effect of leptin in intestinal inflammation is mediated by corticosteroids we performed adrenalectomy experiments in db/db and wild-type mice. Our results suggested that the diminished intestinal response to toxin A in db/db mice was related only in part to increased levels of corticosteroids. CONCLUSIONS: Leptin plays an important role in regulating the severity of enterotoxin-mediated intestinal secretion and inflammation by activating both corticosteroid-dependent and -independent mechanisms.

Animals↗
PubMed1980

Water and electrolyte movement and mucosal morphology in the jejunum of patients with portal hypertension.

Intestinal secretion and intercullular space dilatation can be induced in animal models by acute elevation of intravascular volume or portal pressure. We examined whether patients with increased portal venous pressure might represent a clinical counterpart to these animal models. Portal venous pressure, determined by hepatic wedge pressure measurement, was elevated to 10-55 mmHg (mean 29 mmHg) in 8 patients with chronic liver disease without diarrhea. Intestinal transport studies utilizing a steady-state perfusion technique revealed normal absorption of a plasmalike electrolyte solution. A solution dsigned to unmask intestinal secretion demonstrated no difference from control subjects in the movement of water, electrolytes, or protein into the intestional lumen. There was no correlation of absorption of secretion with hepatic wedge pressure. Jejunal biopsy revealed a significant increase in dilatation of intercellular spaces in patients compared to controls; this increase was not correlated with hepatic wedge pressure, but was significantly inversely correlated to plasma renin and aldosterone concentration. We conclude that patients with chronic liver disease and portal hypertension absorb water and electrolytes normally, but have mild morphologic alterations in the intestinal mucosa, possibly related to intravascular volume status.

Adult↗
PubMed1983

Transport characteristics of p-acetamidobenzoic acid in brush border membrane of rat small intestine.

Brush border membrane vesicles of rat small intestinal mucosa were prepared by the modified calcium precipitation method in order to investigate the intestinal secretion mechanism of p-acetamidobenzoic acid (Ac-PABA). The release rate of [14C]-Ac-PABA from preloaded vesicles was much faster than that of p-aminobenzoic acid (PABA) and was enhanced by the addition of unlabelled Ac-PABA in the outer medium. In contrast, the membrane transfer rate of Ac-PABA across the egg lecithin liposomes was slower than that of PABA. The contribution of a carrier-mediated transport mechanism in the brush border membrane to the intestinal secretion of Ac-PABA was suggested.

4-Aminobenzoic Acid↗