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At least 955 records · Page 53Linked to original sources
PubMed1978

[Conservative treatment of intestinal obstruction: prospects and limits. Experiences with 27 cases treated by Miller-Abbott-tubes inserted endoscopically (author's transl)].

27 cases of intestinal obstruction primarily treated conservatively by means of Miller-Abbott-tubes are presented, technical details, clinical results, indications and risks of the procedure discussed. The controlled placement of the tube using a gastroscope rules out technical failures. Fifteen patients were cured, 2 patients removed the tube; in 8 cases the procedure turned out to be ineffective; they were cured by laparotomy. The separate monitoring of gastric and intestinal secretion permits early prognosis in respect to efficacy. Two patients died. Strict limitation of indication is of decisive importance. The method is highly effective in early postoperative intestinal obstruction--apparently of mechanical as well as of paralytic origin. In our experience, the possible mistaking of anastomotic leakage for postoperative ileus is practically negligible. For acute admissions with intestinal obstruction of unclear origin, however, the procedure should only be aimed at the resotration of general condition before surgery. In spite of the fact, that some cases of late postoperative intestinal obstruction could be cured conservatively, the risk of delaying operations of utmost necessity in cases of strangulation, incarceration and perforation is too high.

Adolescent↗
PubMed2006

Humoral response of chicken infected with the microsporidium Encephalitozoon hellem.

Chicken (Gallus gallus) were used as the experimental model for study of immune response against the microsporidium Encephalitozoon hellem (Didier et al., J Inf Dis 163:617-621, 1991) infection in birds. Two-day-old chicken were infected perorally or intraperitoneally with a dose of 10(7) spores of E. hellem. The anti-E. hellem immunoglobulin (Ig)A, IgY, and IgM antibody responses in sera and dropping sample extracts were determined by enzyme-linked immunosorbent assay. Results have shown specific antibody production in sera and intestinal secretions of infected birds. Chicken inoculated perorally developed the lowest antibody response. Microsporidian spores were not identified in the smears from cloacal swab samples of individual chicken. Intestinal segment cultures of perorally infected chicken cultivated in vitro showed the highest production of specific IgY and IgA antibodies in jejunum segments. In the further course of infection, the colon produced the highest amount of IgA, and the ileum and colon produced the highest amount of IgY.

Animals↗
PubMed1986

Production and utilization of a mouse monoclonal antibody to rat IgA: identification of gender-related differences in the secretory immune system.

The present study was designed: to produce a mouse monoclonal antibody to rat IgA; and to examine, by using the monoclonal antibody, possible gender-related differences in the secretory immune system. Hybridomas were prepared that secreted mouse monoclonal antibodies directed specifically against rat IgA. These antibodies were identified as IgG1 and kappa chain positive and could be used to purify rat IgA by affinity chromatography, detect tissue IgA by immunofluorescence and measure IgA levels in external secretions by radioimmunoassay. In utilizing these antibodies, we found that a distinct, gender-related difference exists in the number of IgA-containing cells in the rat lacrimal gland. Lacrimal tissue from male rats had a significantly higher content of IgA-positive cells than did that from female rats. This difference correlated well with our previous observations on the sexual dimorphism in tear IgA levels. We also observed in the present study that gender-associated variations in IgA content occur in respiratory secretions. In contrast to the eye, however, females had significantly greater IgA concentrations than did males. No effect of gender was found on IgA levels in small intestinal secretions, saliva or serum. Overall, our results indicate that gender may play a role in the immune response of specific mucosal tissues.

Animals↗
PubMed1987

Atrial natriuretic factor receptor heterogeneity and stimulation of particulate guanylate cyclase and cyclic GMP accumulation.

Since the seminal discovery by deBold that atria contain factors that produce diuresis and natriuresis, the biologic effects attributed to ANF have expanded to the point where the name "atrial natriuretic factor" seems inappropriate. In addition to promoting diuresis and natriuresis, ANF has been shown to produce vascular smooth muscle relaxation and to inhibit the secretion of aldosterone from the adrenal cortex, renin from the juxtaglomerlular apparatus, vasopressin from the hypothalamus, and salt and water intake after central administration. ANF also promotes intestinal secretion and stimulates testosterone synthesis in Leydig cells. However, the cellular mechanisms whereby ANF elicits these diverse effects are poorly understood. ANF has been reported to inhibit adenylate cyclase in a number of tissues. However, the significance of ANF inhibition of adenylate cyclase is unknown. This effect cannot be associated with vascular relaxation since decreased cyclic AMP would be expected to promote contraction rather than relaxation. ANF inhibition of adenylate cyclase may mediate the inhibitory effects of ANF on hormone secretion from the anterior pituitary gland. The inhibition of adenylate cyclase could also explain the inhibitory effect of ANF on aldosterone synthesis, since agents that stimulate cyclic AMP increase aldosterone synthesis. However, ANF also inhibits the dibutyryl-cyclic AMP-induced stimulation of aldosterone secretion, suggesting that an inhibition of adenylate cyclase cannot account fully for the inhibitory effects of ANF on aldosterone synthesis. There is no evidence to support a role for cyclic AMP in the diuretic and natriuretic action of ANF. An inhibition of membrane phosphoinositide breakdown by ANF and the subsequent formation of IP3 and intracellular calcium release could explain the inhibitory effects of ANF on vascular contraction and steroid synthesis. However, there is very little evidence to suggest that ANF regulates phosphoinositide metabolism, while some recent studies suggest that ANF may regulate calcium fluxes in vascular tissue. Clearly, cyclic GMP has emerged as the most likely intracellular mediator of ANF effects. ANF increases cyclic GMP in a wide range of tissues by selectively activating particulate guanylate cyclase. However, it is not known which effects of ANF are mediated by cyclic GMP. The discovery that ANF increases cyclic GMP in vascular tissue clearly suggests that cyclic GMP mediates the vascular relaxation effect of ANF, since other classes of vasodilators also increase cyclic GMP. There is preliminary evidence that cyclic GMP may inhibit renin secretion and sodium transport in kidney cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Adenylyl Cyclases↗
PubMed2000

Enterotoxins and the enteric nervous system--a fatal attraction.

Although there has been extensive investigation of the biochemical consequences of the interactions between bacterial enterotoxins and intestinal epithelial cells and the mechanisms by which they induce intestinal secretion, relatively little attention has been given to other aspects of the host response to these enterotoxins. There is now compelling evidence that the enteric nervous system has a major role in enhancing the secretory state induced by cholera toxin, the E. coli enterotoxins and possibly C. difficile toxin A. Cholera toxin for example is thought to activate a neural reflex via the release of 5-hydroxytryptamine from enterochromaffin cells. Neurotransmitters involved in the reflex include substance P and vasoactive intestinal polypeptide. Delineation of these neural pathways may offer new possibilities for the pharmacological control of enterotoxin-mediated secretion.

Animals↗
PubMed1992

Pituitary adenylate cyclase-activating polypeptide stimulates secretion in T84 cells.

Pituitary adenylate-cyclase-activating peptide (PA-CAP) and PACAP-27 are novel hypothalamic peptides that can stimulate adenylate cyclase in cultured anterior pituitary cells. Because these peptides are present in the gut and are homologous with vasoactive intestinal peptide (VIP), itself known to stimulate intestinal ion transport, we examined the effects of these peptides on the T84 colonocyte cell line. Using cells grown on semipermeable supports and mounted in Ussing chambers, we showed that PACAP and PACAP-27 potently activate intestinal secretion. The half-maximal secretory response was produced with 0.5 nmol/L PA-CAP and 0.1 nmol/L PACAP-27. PACAP resembled VIP in that it stimulated a secretory response potentiated by carbachol, inhibited by bumetanide and barium chloride, and not further stimulated by the subsequent addition of VIP. Like VIP, PACAP also stimulated 5' cyclic adenosine monophosphate (cAMP) production and the phosphorylation of cellular proteins known to be substrates for cAMP-dependent protein kinase. In addition, PACAP inhibited 125I-VIP binding to T84 cells, and the secretion it stimulated was reduced by the VIP receptor antagonist, L-8-K. Thus PACAP and PACAP-27 potently stimulate colonocyte ion transport via mechanisms mediated by the VIP receptor and cAMP-dependent signaling.

Cell Line↗
PubMed1970

Elevated concentration of adenosine 3':5'-cyclic monophosphate in intestinal mucosa after treatment with cholera toxin.

A heat-labile factor in cell-free filtrate of a Vibrio cholerae culture induces a marked rise in the wet-weight concentration of adenosine 3':5'-cyclic monophosphate (cyclic AMP) in the intestinal mucosa of the dog. The increase becomes appreciable 1-1.5 hr after intraluminal administration of the filtrate, about the same time as the onset of intestinal secretion in response to a heat-labile enterotoxin in the filtrate. These results are consistent with the hypothesis that cyclic AMP may be an intermediary in the intestinal secretory response to cholera toxin.

Animals↗
PubMed1979

Jejunal secretion in response to a duodenal mixed nutrient perfusion.

A multilumen balloon tube constructed to separate duodenal and jejunal perfusion segments was placed in the proximal small bowel of 6 healthy volunteers. The effect of nutrient mixture in the duodenum on net jejunal water and electrolyte flux was then determined. The duodenum was perfused with a balanced electrolyte solution before and after the nutrient perfusion. Net water flux in the perfused jejunum changed from absorption 27.0 +/- 6.0 microliter/min/cm, (mean +/- SEM) to secretion 7.7 +/- 7.3 microliter/min/cm (P less than 0.025) during nutrient perfusion. There was also net chloride secretion and decreased net absorption of Na, K, and HCO3 (P less than 0.05). The jejunal absorption of water and electrolytes before and after the duodenal nutrient perfusion was the same. Results indicate that intestinal secretion may occur under physiologic conditions at sites remote to the application of food in humans.

Adult↗
PubMed1999

Bacillus thuringiensis Cry1Ac protoxin is a potent systemic and mucosal adjuvant.

Recently we demonstrated that recombinant Cry1Ac protoxin from Bacillus thuringiensis is a potent systemic and mucosal immunogen. In this study we compared the adjuvant effects of Cry1Ac and cholera toxin (CT) for the hepatitis B surface antigen (HBsAg) and bovine serum albumin (BSA). The antibody responses of intestinal secretions and serum were determined by ELISA in Balb/c mice immunized through the intragastric (IG) or intraperitoneal (IP) routes. When HBsAg was administered via IG, the anti-HBsAg intestinal response was not enhanced by either Cry1Ac or CT, whereas via IP Cry1Ac increased the anti-HBsAg intestinal immunoglobulin (Ig)G response and CT increased the intestinal IgA and IgM responses. Serum anti-BSA antibodies increased when BSA was co-administered with CT or Cry1Ac by both routes. Cholera toxin and Cry1Ac co-administered via IP increased the IgG anti-BSA response in fluid of the large intestine and CT also increased the IgA and IgM responses slightly. When co-administered via IP, CT and Cry1Ac did not affect the IgG anti-BSA response of the small intestine significantly. We conclude that Cry1Ac is a mucosal and systemic adjuvant as potent as CT which enhances mostly serum and intestinal IgG antibody responses, especially at the large intestine, and its effects depend on the route and antigen used. These features make Cry1Ac of potential use as carrier and/or adjuvant in mucosal and parenteral vaccines.

Adjuvants, Immunologic↗
PubMed1997

Evidence for a role of the gut hormone PYY in the regulation of intestinal fatty acid-binding protein transcripts in differentiated subpopulations of intestinal epithelial cell hybrids.

Peptide tyrosine tyrosine (PYY) is a gut hormone present in endocrine cells in the lower intestine that can be released by the presence of luminal free fatty acids (FFAs). The biological action of this peptide includes inhibition of gut motility and gastrointestinal and pancreatic secretions. Intestinal fatty acid-binding protein (I-FABP) binds FFA and may be involved in their cytosolic trafficking. Quantitative in situ hybridization on heterogeneous populations of small intestinal somatic cell hybrids selected for endogenous I-FABP expression (hBRIE 380i cells) demonstrated a 5-fold increase in I-FABP transcripts in response to PYY (within 6 h) that was confined to clusters of differentiated cells, whereas ribonuclease protection assays performed on heterogeneous populations of these cells showed no significant differences. High affinity PYY receptors, with an IC50 of 5-50 pM, were identified in both differentiated and nondifferentiated cell populations, as determined by competitive binding assays and autoradiography. In situ hybridization of rat ileal tissue also revealed differing patterns of mRNA expression for liver fatty acid-binding protein (L-FABP) and I-FABP. Only I-FABP mRNA was detected in the villus tips. This localization correlated with the expression pattern of I-FABP mRNA in the hBRIE 380i cells where changes in transcripts were observed only in differentiated cells that did not incorporate bromodeoxyuridine. The sustained expression of I-FABP transcripts in the villar tips suggests (unlike L-FABP) that older terminally differentiated cell populations of the mucosa can still be PYY responsive. These studies demonstrate that physiological concentrations of PYY can regulate I-FABP and place this peptide in a key position as part of a feedback system that determines the processing of cytosolic FFA in the enterocyte. In addition, these studies suggest a mechanism whereby luminal agents can modulate expression of proteins in terminally differentiated cells in the gastrointestinal mucosa.

Animals↗
PubMed1989

Immunoglobulin secretion by isolated intestinal lymphocytes: spontaneous production and T-cell regulation in normal small intestine and in patients with coeliac disease.

The in vitro secretion of immunoglobulins by small intestinal lymphocytes isolated from 47 patients with normal histology and 23 patients with treated and untreated coeliac disease was examined using an enzyme linked immunosorbent assay. In control patients, duodenal lymphocytes spontaneously secreted higher levels of IgM than jejunal lymphocytes (p less than 0.05). Significantly higher levels of both IgA (p less than 0.05) and IgM (p less than 0.001) were secreted by jejunal lymphocytes of 10 patients with untreated coeliac disease than cells isolated from normal jejunal tissue. IgM and IgA secretion by duodenal lymphocytes isolated from control patients was increased in a dose dependent manner by coculture with autologous peripheral blood T lymphocytes. This effect was not observed with jejunal lymphocytes of control or treated coeliac patients. Peripheral T-cells of untreated coeliac patients, however, showed significant helper effects (p less than 0.05) for IgM and IgA secretion by autologous jejunal lymphocytes. The results suggest that jejunal lymphocytes of patients with untreated coeliac disease show major differences in their capacity to synthesise and secrete immunoglobulins in vitro and the enhanced secretion might result from changes in T-cell immunoregulatory function.

Adolescent↗
PubMed1998

Apo B100-containing lipoproteins are secreted by the heart.

The apo B gene is expressed in the human heart and in the hearts of human apo B transgenic mice generated with large genomic clones spanning the human apo B gene. [35S]Methionine metabolic labeling experiments demonstrated that apo B100-containing lipoproteins are secreted by human heart tissue and by human apo B transgenic and nontransgenic mouse heart tissue. Density gradient analysis revealed that most of the secreted heart lipoproteins were LDLs, even when the labeling experiments were performed in the presence of tetrahydrolipstatin, an inhibitor of lipoprotein lipase. Western blots with a microsomal triglyceride transfer protein) (MTP)-specific antiserum demonstrated that the microsomes of the heart contain the 97-kD subunit of MTP (the subunit involved in the transfer of lipids and assembly of lipoproteins). Metabolic labeling of mouse heart tissue in the presence of BMS-192951, an MTP inhibitor, abolished lipoprotein secretion by the heart but resulted in the secretion of two apo B proteolytic fragments (80 and 120 kD), which were found in the bottom fraction of the density gradient. These studies reveal that the heart, and not just the liver and intestine, secretes apo B-containing lipoproteins. We speculate that lipoprotein secretion by the heart represents a mechanism for removing excess lipids from the heart.

Animals↗
PubMed2001

Pathogenesis of rotavirus gastroenteritis.

The outcome of intestinal infection with rotaviruses is more complex than initially appreciated, and it is affected by a complex interplay of host and viral factors. Rotaviruses infect intestinal enterocytes, and the early events in infection are mediated by virus-epithelial cell interactions. Diarrhoea may be caused by several mechanisms including (i) malabsorption that occurs secondary to the destruction of enterocytes, (ii) villus ischaemia and activation of the enteric nervous system that may be evoked by release of a vasoactive agent from infected epithelial cells in the absence of significant pathologic lesions or enterocyte damage, and (iii) intestinal secretion stimulated by the intracellular or extracellular action of the rotavirus non-structural protein, NSP4, a novel enterotoxin and secretory agonist with pleiotropic properties. New studies of rotavirus infection of polarized intestinal epithelial cells show that rotaviruses infect cells differently depending on whether or not they require sialic acid for initial binding, and infection alters epithelial cell functions. NSP4 also affects epithelial cell function and interactions. NSP4 (i) induces an age- and dose-dependent diarrhoeal response in young rodents that is similar to virus-induced disease, (ii) stimulates a Ca(2+)-dependent cell permeability where the secretory response is age-dependent, and (iii) alters epithelial cell integrity. Antibody to NSP4 protects mouse pups from diarrhoea induced by homotypic and heterotypic viruses. These data support a new mechanism of rotavirus-induced diarrhoea whereby a viral enterotoxin triggers a signal transduction pathway that alters epithelial cell permeability and chloride secretion. This new information about how a gastrointestinal virus causes disease demonstrates common pathogenic mechanisms for viral and bacterial pathogens not previously appreciated. These results also suggest new approaches to prevent or treat rotavirus-induced diarrhoea.

Animals↗
PubMed1989

Single chloride channels in colon mucosa and isolated colonic enterocytes of the rat.

Chloride channels from rat colonic enterocytes were studied using the patch-clamp technique. After removal of mucus, inside-out patches were excised from the apical membrane of intact epithelium located at the luminal surface. They contained spontaneously switching Cl- channels with a conductance of 35-40 pS. The channels were blocked reversibly by anthracene-9-carboxylic acid (1mM). In excised patches from single enterocytes, isolated by calcium removal, the Cl- channels were studied in more detail. The I-V relation was linear between +/- 80 mV. The selectivity was I- greater than Br- greater than Cl- = NO3- greater than F- = HCO3-. Thirty pS Cl- channels were also found on the basolateral membrane of crypts isolated by brief calcium removal. The I-V curve of these Cl- channels was also linear. The results provide direct evidence for the existence of Cl- channels in the apical membrane of surface cells in colonic mucosa. The properties of these channels are similar to those previously observed when incorporating membrane vesicles into planar lipid bilayers. Both results support the validity of the theoretical models describing intestinal secretion.

Animals↗
PubMed2000

Eicosanoids and the small intestine.

Prostaglandins play an important role in modulation of various physiologic processes in the small intestine. In this review, the involvement of prostaglandins in various small-intestinal functions including small-intestinal secretion, mucosal protection, epithelial and endothelial barrier function, and motility are discussed.

Animals↗
PubMed2004

Stimulation of colonic anion secretion by monochloramine: action sites.

During inflammatory bowel disease, reactive oxygen metabolites are released by phagocytes reacting with intraluminal NH3 to produce monochloramine (NH2Cl). NH2Cl is assumed to play role in the pathogenesis of inflammation-associated diarrhoea, as it is able to induce intestinal secretion. The aim of the present study was to determine the action sites of NH2Cl in rat colonic epithelium with Ussing chamber and fura-2 experiments. In intact mucosa, NH2Cl (5.10(-6)-10(-4) mol.l(-1)) evoked a concentration-dependent increase in short-circuit current (Isc), consistent with the induction of anion secretion, as demonstrated by anion substitution and transport blocker experiments. When the apical membrane was permeabilised by the ionophore nystatin, two basolateral action sites of NH2Cl (5.10(-5) mol.l(-1)) could be identified, i.e. an increase in the K+ conductance and a stimulation of the Na+-K+ pump. When tissues were basolaterally depolarised by a high K+ concentration, the stimulation of an apical Cl- conductance by NH2Cl was observed. In isolated colonic crypts loaded with the Ca2+-sensitive fluorescent dye fura-2, NH2Cl (5.10(-5) mol.l(-1)) evoked an increase in the intracellular Ca2+ concentration. This increase was independent from the presence of Ca2+ in the extracellular medium, but was inhibited by blockade of intracellular sarcoplasmatic, endoplasmatic Ca2+-ATPases with cyclopiazonic acid (10(-5) mol.l(-1)). The NH2Cl-evoked Ca2+ release was sensitive against inhibition of ryanodine receptors with ruthenium red (5.10(-5) mol.l(-1)) and against inhibition of inositol-1,4,5-trisphosphate (IP3) receptors with 2-aminoethoxydiphenylborate (10(-4) mol.l(-1)). Both blockers also inhibited the NH2Cl-induced increase in Isc. These results indicate that an intracellular Ca2+ release via ryanodine and/or IP3 receptors is involved in oxidant stimulation of anion secretion in rat colon.

Ammonium Chloride↗
PubMed1982

Calcium metabolism in young rats during early dietary phosphate deprivation.

A series of in vivo experiments were designed to study the early effects of phosphate depletion on calcium metabolism in young adult (8-10 week old) rats with intact thyroid--parathyroid glands. Hypercalciuria occurred within 24 h of dietary phosphate deprivation. It was the consequence of mobilization of calcium stores from the exchangeable calcium pool of the diaphysis of bone. Increased net intestinal absorption of calcium also occurred early. This was at least in part due to decreased net intestinal secretion of calcium into the gut lumen. Thus the early onset of hypercalciuria and hypercalcemia associated with Pi deprivation in normal growing young rats is the combined result of increased net intestinal calcium absorption and increased calcium mobilization from bone.

Age Factors↗
PubMed2002

[Enterotoxigenic Bacteroides fragilis as a factor in diarrhea].

The etiology of almost half of the diarrheal diseases has not been cleared yet, in spite of modern diagnostic methods. Bacteroides fragilis strains which secrete an enterotoxin are termed as enterotoxigenic B.fragilis (ETBF). These strains are associated with diarrheal diseases in children above 1 year of age and in adults. B. fragilis toxin (BFT) stimulates intestinal secretion and in-vitro cytotoxic response in HT29/C1 cells. Recent studies suggest that BFT is related to inflammatory bowel disease and colon cancer by triggering nuclear activation with potential oncogene expression. In this review, the molecular pathogenesis, epidemiology and laboratory diagnosis of ETBF have been reviewed to focus on ETBF as a diarrheal agent.

Bacteroides Infections↗