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At least 451 records · Page 25Linked to original sources
PubMed1994

Regulation of glucagon-like peptide-1-(7-36) amide secretion by intestinal neurotransmitters and hormones in the isolated vascularly perfused rat colon.

Glucagon-like peptide-1 (GLP-1) is promptly released from endocrine cells of the distal part of the gut after oral ingestion of a meal. To test the possibility that hormones produced by the proximal small intestine or transmitters of the enteric nervous system may be involved in the early phase of meal-induced GLP-1 secretion, various intestinal regulatory peptides and neurotransmitters of the gut were administered intraarterially in the isolated vascularly perfused rat colon preparation. The release of GLP-1 in the portal effluent was measured by a specific RIA. Intraarterial infusion of glucose-dependent insulinotropic peptide (GIP) over the concentration range 0.25-1 nM evoked a dose-dependent release of GLP-1, with a maximal response of 350% of the basal value. Tetrodotoxin did not modify the GIP-induced release of GLP-1. Secretin or cholecystokinin did not stimulate the secretion of GLP-1. Bombesin (10(-9)-10(-7) M) provoked a dose-dependent release of GLP-1, consisting of an early peak, followed by a sustained response. Calcitonin gene-related peptide (5 x 10(-8) M) induced a dramatic rise of GLP-1 immunoreactivity in the portal effluent (peak at 800% of the basal value 10 min after the start of infusion). Similarly, the beta-adrenergic agonist isoproterenol at concentrations of 10(-7) and 10(-6) M provoked a pronounced release of GLP-1 (peak at 500% of the basal value with 10(-6) M isoproterenol). Finally, the muscarinic cholinergic agonist bethanechol at a concentration of 10(-4) M evoked a gradual increase in GLP-1 immunoreactivity, which reached a maximal value (900% over basal) at the end of the 30-min infusion period. The lowest concentration of bethanechol used in the present study (10(-5) M) did not increase portal GLP-1 immunoreactivity over the basal value. Tetrodotoxin did not modify the bethanechol-, isoproterenol-, calcitonin gene-related peptide-, or bombesin-induced GLP-1 release. In conclusion, the present study conducted with the isolated vascularly perfused rat colon shows that there are interactions between the two most potent incretins, GIP and GLP-1, probably through an enteroendocrine pathway. Additionally, several transmitters of the gut are potent stimulants of GLP-1 release and, therefore, represent potential tools in the treatment of the noninsulin-dependent diabetes mellitus.

Animals↗
PubMed1982

5-hydroxytryptamine and cholera secretion. Physiological and pharmacological studies in cats and rats.

The intestinal secretion evoked by close intra-arterial infusion of 5-hydroxytryptamine (5-HT) in cats was inhibited by tetrodotoxin, a drug abolishing action potentials. Furthermore, the intestinal secretion produced by placing a 2-mM 5-HT solution in the intestinal lumen of rats was inhibited by hexamethonium, a ganglionic receptor-blocking agent. These observations strongly indicate that 5-HT-induced secretion is, at least in part, neurally mediated. It was also shown that 5-HT receptors are involved in the pathophysiology of choleraic secretion, since the secretion was inhibited by making the experimental animal tachyphylactic against 5-HT. No effects of 5-HT tachyphylaxis were noted on fluid transport in normal intestines. The results are discussed in relation to a new hypothesis for the pathophysiology of cholera secretion.

Animals↗
PubMed1986

Secretory IgA specific for Toxoplasma gondii.

Secretory IgA specific for Toxoplasma gondii was identified in intestinal secretions of mice infected perorally with bradyzoites (encysted in brain) of the Me49 strain of T. gondii by using immunofluorescence microscopy and an ELISA. This activity was absorbed with tachyzoites of T. gondii but not mouse brain. To determine whether increased total amount of intestinal IgA might cause a nonspecific reaction in the ELISA for T. gondii-specific IgA, mice were immunized perorally with cholera toxin. This immunization produced intestinal IgA antibody to cholera toxin and increased the total amount of intestinal IgA, but there was no reactivity of intestinal secretions in the ELISA for T. gondii-specific IgA. Experiments in which ELISA were performed with monoclonal IgA, IgG, or IgM and antisera to IgA, IgG, or IgM demonstrated that the ELISA was specific for each Ig class. In addition, monoclonal IgA competed with the anti-Toxoplasma IgA activity of intestinal secretions obtained from mice infected with T. gondii.

Administration, Oral↗
PubMed1999

Preferential enhancement of B cell IgA secretion by intestinal epithelial cell-derived cytokines and interleukin-2.

Intestinal epithelial cells (IEC) are known to secrete a number of important cytokines. Recently, we determined that IEC-derived IL-6 and TGF-beta could enhance IgA secretion and suppress IgM secretion by isolated mucosal B cells. However, since the IEC-derived cytokines must function in the context of locally produced T cell cytokines, the effect of IEC- and T cell-derived cytokines on mucosal B cell immunoglobulin secretion was determined. Using 4 day culture supernatants (IEC-SN) from the rat IEC-6 intestinal epithelial cell line and lipopolysaccharide (LPS) stimulated Peyer's patch or mesenteric lymph node B cells, the IEC- SN was found to act with IL-2 to greatly enhance IgA secretion but limit or suppress IgM secretion as compared to cultures of LPS stimulated B cells alone. However, neither IL-4, IL- 5, nor IFN-gamma affected IgA secretion with the IEC-SN. Depletion of the IEC-SN with specific anti-cytokine antibodies suggested that IEC-derived TGF-beta and IL-6 were both responsible for the enhancing effect along with IL-2 on IgA secretion, whereas IEC-derived TGF-beta alone limited or suppressed IgM secretion. These results suggest that cytokines derived from local IEC and T cells may create an environment which may contribute to the preferential enhancement of IgA secretion seen in mucosal tissues.

Animals↗
PubMed1998

Nutrient and peptide regulation of somatostatin-28 secretion from intestinal cultures.

Of the two known forms of intestinal somatostatin, somatostatin-28 (S28) and S14, S28 predominates in the distal mucosa, whereas S14 is localized in the foregut. Although S14 release has been well studied, little is known about the factors regulating secretion of S28 from the intestine. Therefore, fetal rat intestinal cultures, which have been previously demonstrated to synthesize and secrete predominantly S28, were treated with potential nutrient, neuromodulator/transmitter, and peptide secretagogues (n = 4-6/experiment). Oleic acid dose dependently stimulated the release of somatostatin-like immunoreactivity (SLI) to 272 +/- 81% of the control value at 1.5 x 10(-4) M (P < 0.01). Gel permeation analysis (n = 3) demonstrated that this increment was accounted for not only by an increase in the release of S28, but also by an increase in that of S14, such that the secretion of both peptides was increased in parallel. Of the neuromodulators tested, only the enteric peptide gastrin-releasing peptide stimulated intestinal SLI secretion, to 386 +/- 60% of the control value at 10(-6) M (P < 0.001); similar to oleic acid, the effects on S28 and S14 were equivalent. Galanin, vasoactive intestinal peptide, bethanechol, and epinephrine did not affect SLI release. The duodenal hormone secretin also stimulated SLI release to 310 +/- 78% of the control value at 10(-6) M (P < 0.001); however, secretin caused a preferential release of S14 over that of S28 (S14, 7.8 +/- 2.8-fold; S28, 1.5 +/- 0.1-fold). In contrast, gastrin, cholecystokinin, glucose-dependent insulinotropic peptide, neurotensin, peptide YY, epidermal growth factor, and transforming growth factor-alpha had no effect on intestinal SLI release. Thus, luminal nutrients and neuro/endocrine peptides exert differential effects on S28 release from the rat intestine compared with those on S14. These findings implicate S28 as a distinct regulatory peptide in the physiological setting.

Animals↗
PubMed2002

Systemic and intestinal antibody secreting cell responses and protection in gnotobiotic pigs immunized orally with attenuated Wa human rotavirus and Wa 2/6-rotavirus-like-particles associated with immunostimulating complexes.

The undesirable side effects and variable efficacy of some oral live rotavirus vaccines in infants have necessitated alternative vaccine approaches. We evaluated a recombinant RFVP2/WaVP6 rotavirus-like-particle (2/6VLP) oral vaccine, using an immunostimulating complex (ISCOM) matrix as adjuvant, in a gnotobiotic (Gn) pig model of human rotavirus (HRV) disease. The 2/6VLPs adhered to the ISCOM-matrix (2/6VLP-ISCOM ) and were antigenic, but they failed to induce protection. However, when combined with attenuated (Att) HRV for oral priming, the 2/6VLP-ISCOM vaccine was effective as a booster and induced partial protection against virulent Wa HRV. The 250 microg 2/6VLP dose was more effective than 100 microg. The highest mean numbers of IgA antibody secreting cells evaluated by ELISPOT in intestinal lymphoid tissues were in pigs receiving AttHRV+2/6VLP-ISCOM or three doses of AttHRV and were associated with the highest protection rates.

Administration, Oral↗
PubMed1985

Phorbol ester stimulation of active anion secretion in intestine.

Phorbol 12,13-dibutyrate (PDB) stimulates electrogenic anion secretion in rabbit and chicken distal ileum. The 50% effective dose in each case was 15 nM, and the maximal short-circuit current (Isc) responses seen at 10(-6) M were 20 and 140 microA/cm2, respectively. Isc was also stimulated by the diacylglycerol 1-oleoyl-2-acetyl glycerol (10(-5) M) but not by the inactive phorbol ester analogue 4 alpha-phorbol 12,13-didecanoate. Removal of Ca from the serosal bathing medium and pretreatment of tissues with atropine (10(-6) M) or tetrodotoxin (2 X 10(-7) M) did not affect PDB-stimulated responses. PDB also did not alter basal intracellular free Ca levels in isolated chicken enterocytes loaded with quin 2 or basal adenosine 3',5'-cyclic monophosphate levels in intact tissues from rabbit and chicken. In the presence of PDB, Ca- and phospholipid-dependent phosphorylation of several proteins in particulate and soluble fractions from isolated chicken enterocytes were seen. Pretreatment of chicken and rabbit tissues with indomethacin or mepacrine inhibited the Isc responses to PDB and carbamylcholine, suggesting a role for prostaglandins. These results suggest that electrogenic anion secretion stimulated by phorbol esters and diacylglycerol may be mediated by activation of protein kinase C.

Animals↗
PubMed1989

Effect of misoprostol in preventing stress-induced intestinal fluid secretion in rats.

Psychological stress may alter gastrointestinal function by central nervous system controlled alteration of local intestinal mediators. Prostaglandins have been shown to prevent epithelial damage to various noxious stimuli. The purpose of this study was to determine (a) if wrap restraint stress altered in vivo intestinal fluid absorption in rats, and (b) if the prostaglandin E1 analogue, misoprostol, could correct observed fluid malabsorption. In vivo loop studies demonstrated net fluid secretion in the ileum and colon of cold wrap restraint stressed rats. In cold wrap restraint stressed rats, misoprostol reversed net secretion to absorption, but it had no effect on fluid absorption in controls. Mild wrap restraint stress did not alter in vivo fluid absorption. We conclude that cold wrap restraint stress is accompanied by net intestinal fluid secretion that can be effectively reversed with misoprostol.

Alprostadil↗
PubMed1986

Quantitative and temporal analyses of murine antibody response in serum and gut secretions to infection with Giardia muris.

We analyzed the appearance and level of Giardia muris-specific antibody of immunoglobulin A (IgA), IgG, and IgM isotypes, at weekly intervals, over the course of a 7-week infection in BALB/c and C57BL/6 mice. Using sensitive immunoradiometric assays, we observed that IgA antibody was the only detectable anti-G. muris antibody in intestinal secretions throughout the course of infection. No secreted IgG or IgM anti-G. muris antibody was detected even in concentrated intestinal secretions. The expulsion of G. muris by the mice was associated closely with the appearance and increasing levels of secreted anti-G. muris IgA antibody. Both IgG and IgA serum antibody to G. muris were detected, but no serum IgM antibody was detected. Serum IgA and IgG anti-G. muris antibody remained at high levels up to 10 weeks following clearance of the parasite. An interesting observation indicated that serum IgA antibody to G. muris developed more slowly in response to infection than secreted IgA antibody. An analysis of the molecular weight distribution of total serum IgA in infected mice determined that infection produced a transient but significant shift in serum IgA to high-molecular-weight (greater than or equal to dimeric IgA) forms. The results indicate that a substantial IgA antibody response occurs in sera and in gut secretions of G. muris-resistant mice and that IgA antibody is the dominant and possibly the only effector antibody active in intestinal secretions during G. muris infection in mice.

Animals↗
PubMed1998

Effects of Hange-shashin-to on cholera toxin-induced fluid secretion in the small intestine of rats.

The effects of Hange-shashin-to (TJ-14) on cholera toxin-induced intestinal fluid secretion were studied to elucidate the mechanism by which this kampo medicine manifests antidiarrheal effects. TJ-14 suppressed the intestinal fluid secretion induced by cholera toxin (1 microg/rat) in a dose-dependent manner at doses between 125 and 1000 mg/kg. It also inhibited the luminal prostaglandin E2 (PGE2) level. On the other hand, serotonin (5-HT) release was not affected by TJ-14. Subcutaneous injection of indomethacin at 10 mg/kg or ondansetron at 100 microg/kg significantly suppressed intestinal secretion. The luminal PGE2 level was also inhibited by indomethacin (10 mg/kg, s.c.). TJ-14, even at 10(-4) g/ml, had little effect on the phasic contraction of isolated guinea pig ileum induced by 5-HT (2 x 10(-6) g/ml), while ondansetron suppressed the phasic contraction caused by 5-HT. These results indicate that TJ-14 is useful in suppressing cholera toxin-stimulated intestinal fluid secretion, and that this effect is partially due to its suppressive action on the PGE2 level.

Animals↗
PubMed1991

Assessment of water and solute absorption from experimental hypotonic and established oral rehydration solutions in secreting rat intestine.

Water and solute absorption from three experimental hypotonic oral rehydration solutions (HYPO-ORS; sodium 45, 60 and 75 mmol/L, glucose 90 mmol/L), the World Health Organization recommended ORS (WHO-ORS; sodium 90 mmol/L, glucose 111 mmol/L), and the British National Formulary recommended ORS (BNF-ORS; sodium 35 mmol/L, glucose 200 mmol/L), have been assessed by perfusion studies in cholera toxin-induced secreting rat intestine. Net water absorption was greatest from the most hypotonic solution (HYPO-45; P less than 0.05). UK-ORS prevented net water secretion and WHO-ORS promoted moderate net water absorption. Net sodium secretion was seen with all solutions but was least from WHO-ORS and greatest with BNF-ORS (P less than 0.01). Glucose absorption was similar from BNF-ORS, WHO-ORS and HYPO-45 and in each case was greater than glucose absorption from HYPO-60 and HYPO-75 (P less than 0.05). These results suggest that net water and sodium absorption from ORS may be enhanced if osmolality is reduced by decreasing the glucose content.

Animals↗
PubMed1986

Tetrodotoxin inhibits directly acting stimulants of intestinal fluid secretion.

Intravenous injection of tetrodotoxin (20 micrograms kg-1) to anaesthetized rats blocks PGE1- and inhibits VIP-induced fluid secretion from the mucosa of the jejunum without affecting the physiological rates of net water and glucose absorption. It is suggested that the toxin might release an endogenous inhibitor of secretion or that it might possess direct antisecretory activity on the epithelial cells of the jejunum. It is further suggested that results where tetrodotoxin has been used to investigate secretagogue action should be treated with caution.

Alprostadil↗
PubMed1994

Giardia muris trophozoite antigenic targets for mouse intestinal IgA antibody.

The aim of this work was to characterize Giardia muris trophozoite proteins that are targets for intestinal anti-trophozoite IgA in G. muris-infected mice. Intestinal secretions were obtained from immunocompetent BALB/c mice that had been infected with G. muris cysts 4-5 weeks previously and from control uninfected BALB/c mice. Flow cytometry of G. muris trophozoites that had been incubated with intestinal secretions and with fluorescein isothiocyanate-conjugated anti-mouse IgA showed that anti-trophozoite IgA was present in intestinal secretions obtained from infected BALB/c mice. By immunoblotting on G. muris trophozoite proteins separated by one-dimensional gel electrophoresis, this IgA recognized at least one trophozoite protein of molecular mass of approximately 80 kDa. The 80-kDa G. muris protein(s) has a molecular mass similar to that described for cysteine-rich surface proteins of the human parasite Giardia lamblia.

Animals↗
PubMed1982

Characteristics of intestinal glucose secretion in normal and diabetic rats.

A method was developed to characterize and quantitate the transfer of glucose from the plasma to the intestinal lumen. In normal rats, there was a linear correlation between the blood glucose concentration and the rate of appearance of plasma glucose into the intestinal lumen perfused with Krebs-Ringer buffer (r = 0.88, P less than 0.01). Intestinal perfusion with buffers containing either mannitol, glucose, or phlorizin significantly increased the recovery of secreted glucose compared with plain buffer. Rats perfused with buffer containing mannitol or those undergoing plasma volume expansion with dextran demonstrated a change in water movement from net absorption to secretion coupled with a significant increase in glucose secretion. During luminal perfusion with a buffer containing 21 mM glucose, glucose secretion represented 14% of the net glucose absorption rate. Intestinal perfusion with phlorizin gave the highest measured recovery of glucose, probably by blocking active reabsorption of secreted glucose. A series of simultaneous perfusions performed in the jejunum and ileum revealed similar rates of glucose transfer in both segments of intestine. Measurement of glucose secretion in rats with streptozotocin diabetes gave the highest values for the plasma-to-lumen movement of glucose. Treatment with insulin reduced the blood sugar and glucose transfer rate. These data demonstrate that glucose moves bidirectionally across the rat intestine, and its secretion is a passive process.

Animals↗
PubMed1989

Effect of Yersinia enterocolitica on intestinal mucin secretion.

Mucin and glycoprotein synthesis and secretion were evaluated in the upper, mid, and distal small intestine and in the proximal colon of rabbits infected with Yersinia enterocolitica (YE). Infected (INF) animals were examined on day 6 and compared with pair-fed controls and unmanipulated weight-matched rabbits. Tissue mucin content in vivo and mucin secretion in vitro, measured by a specific immunoassay, were significantly elevated in all four regions of the gut of INF rabbits compared with both control groups. In vitro secretion of stored glycoprotein, prelabeled with [3H]glucosamine, was not increased in the upper and mid small intestine of INF animals but was significantly elevated in the distal small intestine and proximal colon. In vitro incorporation of [14C]glucosamine was increased in all four regions of the gut of INF rabbits, but secretion of newly synthesized [14C]glycoprotein was only significantly elevated in the distal small intestine and proximal colon. A graded response was observed down the intestinal tract of INF rabbits, with the greatest increase in mucin content, synthesis and secretion occurring in the distal small intestine and proximal colon where the morphological impact of disease is also most severe.

Animals↗
PubMed2005

Brain tumor oncolysis with replication-conditional herpes simplex virus type 1 expressing the prodrug-activating genes, CYP2B1 and secreted human intestinal carboxylesterase, in combination with cyclophosphamide and irinotecan.

The treatment of malignant glioma is currently ineffective. Oncolytic viruses are being explored as a means to selectively lyse tumor cells in the brain. We have engineered a mutant herpes simplex virus type 1 with deletions in the viral UL39 and gamma(1)34.5 genes and an insertion of the two prodrug activating genes, CYP2B1 and secreted human intestinal carboxylesterase. Each of these can convert the inactive prodrugs, cyclophosphamide and irinotecan (CPT-11), into their active metabolites, respectively. This new oncolytic virus (MGH2) displays increased antitumor efficacy against human glioma cells both in vitro and in vivo when combined with cyclophosphamide and CPT-11. Importantly, cyclophosphamide, CPT-11, or the combination of cyclophosphamide and CPT-11 does not significantly affect oncolytic virus replication. Therefore, MGH2 provides effective multimodal therapy for gliomas in preclinical models when combined with these chemotherapy agents.

Antineoplastic Combined Chemotherapy Protocols↗