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At least 811 records · Page 45Linked to original sources
PubMed1989

An investigation of the role of possible neural mechanisms in cholera toxin-induced secretion in rabbit ileal mucosa in vitro.

1. Cholera toxin stimulates intestinal secretion in vitro by activation of mucosal adenylate cyclase. However, it has been proposed that cholera toxin promotes secretion in vivo mainly through an indirect mechanism involving enteric neural reflexes. 2. We examined this hypothesis further by studying the influence of neuronal blockade on cholera toxin-induced changes in fluid transport across rabbit ileum in vitro. Mucosa, stripped of muscle layers, was mounted in flux chambers and luminal application of crude cholera toxin (2 micrograms/ml) caused a delayed but sustained rise in the short-circuit current, electrical potential difference and Cl- secretion. Pretreatment with the nerve-blocking drug, tetrodotoxin (5 x 10(-6) mol/l serosal side), failed to influence the secretory response to cholera toxin, and addition of tetrodotoxin at the peak response to cholera toxin also had no effect. 3. That tetrodotoxin could block neurally mediated secretagogues was confirmed by the demonstration that the electrical responses to neurotensin (10(-7) mol/l and 10(-8) mol/l) were blocked by tetrodotoxin (5 x 10(-6) mol/l). Furthermore, the response to cholera toxin of segments of ileum, which included the myenteric, submucosal and mucosal nerve plexuses, was not inhibited by tetrodotoxin. 4. We conclude that cholera toxin-induced secretion in rabbit ileum in vitro is not mediated via a neurological mechanism.

Animals↗
PubMed2000

Sjögren's syndrome: a possible pathogenetic mechanism involving somatostatin.

Sjögren's syndrome is a chronic systemic disease that primarily affects the salivary and lacrimal glands. The pathogenesis of Sjögren's syndrome is unknown. We hypothesize that reduced somatostatin activity is an important factor in promoting immune dysregulation in patients affected by Sjögren's syndrome. Somatostatin is a multifunctional peptide with potent immunomodulatory properties. Its effects include reduced lymphocytic activity, reduced gastric and intestinal secretions, activation of the hypothalamic-pituitary axis, and anti-inflammatory action, all opposite to the general presentation in Sjögren's syndrome. We suggest that the activity of somatostatin is low in patients affected by this disease, and this contributes significantly to the pathology observed.

Adjuvants, Immunologic↗
PubMedDate not supplied

[Characteristics of intestinal immune response of rats infected with Nippostrongylus brasiliensis].

After infection of rats with Nippostrongylus brasiliensis the response was a synthesis of hemagglutinating antibodies in intestinal secretions, the activity of which is mainly due to IgA. When rats were infected with 83 larvae (which is the smallest immunizing dose), local antibodies were evidenced just after parasite localization had occurred in the gut, whereas serum antibodies were not detected before a challenge infection. Some of these local antibodies were directed against two types of worm antigen which can induce immunity: sevretory antigens and phosphorylcholine. These experiments a role for local antibodies in mechanism of worn expulsion.

Animals↗
PubMedDate not supplied

[Endangering the water-electrolyte balance in gastrointestinal diseases in the aged].

In old people the range of operation, as well as the adaptability of the electrolyte and water metabolism, is reduced by the involutive reduction of the renal, pulmonary and endocrinic functions, as well as by a reduced feeling of thirst, a reduction of the buffer mechanisms, and a dwindling amount of body water. The threat to the maintenance of the requisite amount of body-water and to a normal electrolysis, caused by gastro-intestinal illnesses, is discussed from the point of view of geriatrics. Hydro-mineral upsets occurring in gastroenterology are primarily caused either by an inadequate supply, inadequate absorption, or by an extra-ordinary loss of intestinal secretions, as well as by interference with the normal electrolyte and water metabolism due to medical treatment. Situations in which such hydro-mineral disturbances wright occur are indicated and therapeutic measures suggested. We assert and prove that in old people the danger of extreme reduction of body-water and electrolysis frequently presents a greater threat to life than the illness from which it proceeds, and we maintain that a due consideration of this problem can in many cases literally save the life of the old patient.

Acid-Base Equilibrium↗
PubMed1978

Intestinal contribution to secretion of very low density lipoproteins into plasma.

To resolve the question of the magnitude of the intestine's contribution to circulating very low density lipoproteins (VLDL), measurements of intestinal, hepatic, and total VLDL--triglyceride were made on the same animals or on animals studied under comparable conditions. Animals were examined in the fasted state and during infusion of a fat-free meal. Intestinal VLDL secretion was determined through timed collections of lymph from the mesenteric lymph duct; hepatic and total VLDL secretion rates were estimated by the accumulation of plasma VLDL after injections of Triton WR 1339. Results indicate that the intestine contributes only a minor portion (11%) of the amount of triglyceride entering into the plasma compartment in the fasted state. Although intestinal triglyceride production is increased by 50% (p less than 0.01) in fed rats, the overall contribution of the intestine is not significantly altered in fed rats and represents only 14--17% of total body VLDL secretion. Thus, although intestinal VLDL secretion can be modified experimentally, its total impact on endogenous triglyceride production in normotriglyceridemic rats is small.

Animals↗
PubMed1984

Somatostatin treatment of gastrointestinal fistulas: evidence for a rebound effect on withdrawal.

Three patients with external fistulas from the gastrointestinal tract were treated with somatostatin, a peptide which inhibits pancreatic, gastric and intestinal secretion. Although somatostatin reduced fistula output in two patients and possibly prevented haemorrhage in one, it did not induce fistula closure in any; moreover on withdrawal of somatostatin one patient developed life threatening gastrointestinal haemorrhage and a transient fistula hypersecretion occurred in the others. This experience of somatostatin treatment was less favourable than that previously reported in other small series. Positive nitrogen balance was probably not maintained during treatment in the three patients reported here and in one patient in a previous study in whom somatostatin was ineffective; the peptide may only promote fistula closure in adequately nourished patients.

Abdominal Muscles↗
PubMed1994

Involvement of nitric oxide in the response to 5-hydroxytryptamine in the rat in-vivo.

The involvement of nitric oxide (NO) in the effects of 5-HT on intestinal secretion and cardiovascular function in anaesthetized rats was investigated using NG-nitro-L-arginine methyl ester (L-NAME), a specific NO-synthase antagonist, and its optical isomer D-NAME. L-NAME significantly reduced the prolonged hypotensive response to 5-HT. It also caused a small rightward shift in the colonic 5-HT dose-response curve. This suggests that NO plays a significant role in the prolonged hypotensive response to 5-HT, and may make a small contribution to the secretory response of the colon, but not that of the jejunum, in the rat in-vivo.

Animals↗
PubMed1983

[Determination of immunoglobulins A in the fluids of normal human intestinal perfusion].

Immunoglobulin A (IgA) in intestinal secretions is present in several molecular forms among which dimeric IgA linked to the secretory component (S-IgA) predominates. IgA was measured in jejunal perfusates obtained in nine normal subjects by intraluminal perfusion under a proximal occluding balloon of an isotonic and non antigenic solution. The method associated reverse radial immunodiffusion technique or nephelometry, using human serum as standard with chromatography on a polyacrylamide indubiose column. Chromatography separated IgA between two fractions whose elution ratios were the same as those found with mixtures of pure monomeric IgA and S-IgA. A scale was constructed from the latter, allowing the calculation of the percentages of monomeric IgA and S-IgA present in the jejunal perfusates, and that of their total content of IgA.

Chromatography↗
PubMed1998

Yersinia enterocolitica-induced interleukin-8 secretion by human intestinal epithelial cells depends on cell differentiation.

In response to bacterial entry epithelial cells up-regulate expression and secretion of various proinflammatory cytokines, including interleukin-8 (IL-8). We studied Yersinia enterocolitica O:8-induced IL-8 secretion by intestinal epithelial cells as a function of cell differentiation. For this purpose, human T84 intestinal epithelial cells were grown on permeable supports, which led to the formation of tight monolayers of polarized intestinal epithelial cells. To analyze IL-8 secretion as a function of cell differentiation, T84 monolayers were infected from the apical or basolateral side at different stages of differentiation. Both virulent (plasmid-carrying) and nonvirulent (plasmid-cured) Y. enterocolitica strains invaded nondifferentiated T84 cells from the apical side. Yersinia invasion into T84 cells was followed by secretion of IL-8. After polarized differentiation of T84 cells Y. enterocolitica was no longer able to invade from the apical side or to induce IL-8 secretion by T84 cells. However, Y. enterocolitica invaded and induced IL-8 secretion by polarized T84 cells after infection from the basolateral side. Basolateral invasion required the presence of the Yersinia invasion locus, inv, suggesting beta1 integrin-mediated cell invasion. After basolateral infection, Yersinia-induced IL-8 secretion was not strictly dependent on cell invasion. Thus, although the plasmid-carrying Y. enterocolitica strain did not significantly invade T84 cells, it induced significant IL-8 secretion. Taken together, these data show that Yersinia-triggered IL-8 secretion by intestinal epithelial cells depends on cell differentiation and might be induced by invasion as well as by basolateral adhesion, suggesting that invasion is not essential for triggering IL-8 production. Whether IL-8 secretion is involved in the pathogenesis of Yersinia-induced abscess formation in Peyer's patch tissue remains to be shown.

Cell Differentiation↗
PubMed1986

Bile and milk from cholera toxin treated rats contain a hormone-like factor which inhibits diarrhea induced by the toxin.

Protection against intestinal secretion induced by cholera toxin (CT) was studied in adult and suckling rats. Peroral CT treatment of lactating females protected their suckling offspring against diarrhea. This milk contained a protective antisecretory factor (ASF) as shown by passive peroral or intravenous transfer of the milk to adult, nontreated recipients in which the cholera response was tested in ligated jejunal loops. Bile from CT-treated rats also contained ASF, which was still present 100 days after the last treatment. Although milk and bile from untreated rats contained no ASF, bile from very old untreated rats did. Chemical characterization showed that ASF in bile and milk both had isoelectric points of about 5.0 and molecular weights of about 25,000. These data are similar to those previously obtained for ASF isolated from porcine pituitary glands, and show that the antisecretory activity is unrelated to immunoglobulins.

Age Factors↗
PubMed1982

The effect of chlorpromazine on the function of colonic and ileal mucosa in the anaesthetized rat.

1 The effect of chlorpromazine (Cpz) on the net fluxes of water and sodium in the ileum and colon has been studied in the anaesthetized rat. 2 Under control conditions both the ileum and colon absorbed water and sodium. Cpz (100 mumol/kg, s.c.) had no significant effect on these basal rates of absorption. 3 Intestinal secretion was stimulated by a combination of intra-arterial prostaglandin E1 (PGE1; 10 nmol kg-1 min-1) and intraluminal theophylline (25 mM). A marked potentiation occurred between PGE1 and theophylline in the stimulation of colonic and ileal secretion. 4 In the ileum, a dose-related inhibition of the PGE 1/theophylline-induced changes in the net fluxes of water and sodium was produced by Cpz (0.1 to 100 mumol/kg, s.c.). Under these conditions the inhibition of the secretagogue-induced changes was significant using Cpz at 1 mumol/kg (s.c.) and a dose of Cpz of 100 mumol/kg (s.c.) returned the net fluxes of both water and sodium to basal levels. 5 In the colon, Cpz, at doses of 0.1 and 1 mumol/kg subcutaneously did not inhibit the PGE1/theophylline-induced changes in the net fluxes of water and sodium, and, in contrast with the ileum, significant changes were only obtained with Cpz at 10 mumol/kg. Increasing the dose of Cpz to 100 mumol/kg further inhibited the net flux of sodium, but not that of water in the colon, and in each case the secretagogue-induced changes were not returned to basal levels.

Alprostadil↗
PubMed1975

Enterotoxins of Escherichia coli and vibriocholerae: tools for the molecular biologist.

With the independent discovery in several different laboratories that Vibrio cholerae and heat-labile Escherichia coli enterotoxins activated an enzyme (adenylate cyclase) in small intestinal epithealial cells to cause an enhanced intestinal secretion mediated by cyclic adenosine 3',5'-monophosphate (cyclic AMP), a molecular mechanism was provided for these disease states. As agents that also elevate intracellular concentrations of cyclic AMP in virtually every mammalian tissue tested, the enterotoxins are potentially invaluable tools in investigation of the molecular sequence of events of all cyclic AMP-related cellular phenomena. Cyclic AMP has been known for some time to be the central regulator in the cellular expression of the effects of hormones and has become known more recently as an agent that controls cellular growth by corrdinately influencing several biochemical processes related to rate of cell division. Successful application of the enterotoxins as cellular probes in the areas of regulation of cell division, determination of the reaction mechanism of adenylate cyclase, and elucidation of the relationship between prostaglandin and adenylate cyclase, both in this laboratory and in those of others, is reviewed.

Adenylyl Cyclases↗
PubMed1992

Immunosenescence and mucosal immunity: significant effects of old age on secretory IgA concentrations and intraepithelial lymphocyte counts.

Concentrations of immunoglobulins (Ig) and levels of isotype specific antibodies to three dietary antigens in serum, pure parotid saliva, and in intestinal secretions obtained by whole gut lavage from groups of healthy elderly subjects (aged greater than 70 years) and of younger adult controls (aged 25-50 years) were measured. In addition, counts of lamina propria and intra-epithelial lymphoid cells were performed in histologically normal jejunal biopsy specimens from elderly and younger subjects. Elderly subjects had significantly higher concentrations of serum and salivary IgA and of salivary IgM (both, p less than 0.01), and of salivary IgA antibodies than did the younger subjects, but the amount of immunoglobulin and antibody in whole gut lavage fluid was similar in the two age groups. Jejunal biopsy specimen cell counts showed higher IgA plasma cell counts and lower intraepithelial lymphocyte counts in the elderly group (p less than 0.01), with similar counts of IgM and IgG plasma cells, eosinophils, and mast cells in the two groups. There is evidence of significant effects of old age on the mucosal immune system.

Adult↗
PubMed1984

Cholera toxin feeding did not induce oral tolerance in mice and abrogated oral tolerance to an unrelated protein antigen.

The feeding of protein antigens to mice results in a state of tolerance when feeding is followed by parenteral immunization. Cholera toxin (CT) is a protein that has been used extensively as a potent oral immunogen for mucosal IgA responses, but CT feeding also stimulates a substantial plasma IgG antibody response. This latter finding prompted us to study whether or not CT induces oral tolerance. Mice were fed 5 mg keyhole limpet hemocyanin (KLH) or 10 micrograms CT at least twice before parenteral immunization with 1 microgram KLH or CT in alum i.p. Plasma and intestinal secretions were collected at intervals. The specific IgG or IgA antibody in the samples was measured by ELISA. Although KLH feeding did induce oral tolerance, CT feeding did not induce oral tolerance in any of three mouse strains tested or at any dose of CT given orally. The feeding of the B subunit of CT did not result in oral tolerance either. When both CT and KLH were fed together, CT was able to abrogate oral tolerance to KLH, an antigenically unrelated protein. Moreover, feeding CT along with KLH stimulated secretory IgA anti-KLH responses, whereas no such IgA responses were found when KLH was given alone. Thus, in these experiments with protein antigens, IgA immunization and oral tolerance were reciprocally linked and did not occur simultaneously. CT appears to abrogate oral tolerance and to stimulate secretory IgA responses by altering the regulatory environment in gut-associated lymphoid tissue, shifting it toward responsiveness.

Administration, Oral↗
PubMedDate not supplied

Reduction of fluid-loss in cholera by nicotinic acid: a randomised controlled trial.

A randomised controlled clinical trial was conducted to investigate the ability of nicotinic acid to reduce intestinal secretion in patients with severe cholera. Of the 62 adults investigated, 29 received either 1 or 2 g of nicotinic acid given orally in divided doses and 33 served as controls. Patients who received the 2 g dose had less fluid loss than did their controls during the first (p less than 0.01) and second (p less than 0.05) 8 h post-treatment periods. During the third and fourth 8 h periods, the rates were lower in the treatment groups, but not significantly so. The drug-specific stool reduction was 31%-47% during the first 16 h. Patients receiving 1 g consistently had lower rates of purging than had their controls during each 8 h observation period, but the differences were not significant. The effect of the 2 g dose was significantly better than that with the 1 g dose. The peak inhibition occurred 8-16 h after start of therapy. The drug was well tolerated, the only side-effect being transient flushing of the body in 1 patient.

Adult↗
PubMed1997

In vivo effects of the 5-HT3 antagonist alosetron on basal and cholera toxin-induced secretion in the human jejunum: a segmental perfusion study.

BACKGROUND: 5-hydroxytryptamine type 3 receptor antagonists have been shown to reduce fluid and electrolyte secretion or promote absorption in experimental models of small intestinal secretion. The aim of this study was to compare the effects of a single dose (4 mg) of the 5-hydroxytryptamine type 3 receptor antagonist alosetron and placebo on jejunal fluid and electrolyte movement in humans under basal conditions (n = 7) and following cholera toxin-induced secretion (n = 5) in a randomized, double-blind, crossover design over two separate study periods. METHODS: One hour after oral alosetron or placebo, jejunal intubation was performed. A 30 cm segment of jejunum, isolated by two occluding balloons, was exposed to 15 microg of purified cholera toxin for 2 h prior to triple lumen perfusion with a plasma electrolyte solution containing [14C]-polyethylene glycol as a nonabsorbable volume marker. In the basal study, intestinal perfusion was performed without exposure to cholera toxin. Collection and analysis of the effluent from the jejunal segment allowed fluid and electrolyte movement to be calculated. RESULTS: Alosetron treatment increased basal jejunal fluid absorption (median 5.1 mL/cm/h [interquartile range 4.2 to 7.1] compared with placebo (3.8 [3.6 to 4.3] P = 0.028, two sided Wilcoxon matched pairs signed rank test)). However, following establishment of a secretory state by cholera toxin, alosetron failed to significantly promote absorption or reduce secretion (0.3 [-1.2 to 1.2] compared to placebo (-4.3 [-7.7 to -1.3] P = 0.14)). Adverse events during the study, which included anorexia, nausea, dizziness and loose bowel movements, were not considered to be clinically important. There were no clinically significant changes in laboratory parameters. CONCLUSION: The 5-hydroxytyptamine type 3 receptor antagonist, alosetron, increased basal fluid absorption in normal human small intestine but failed to have a beneficial effect in cholera toxin-induced secretion.

Adult↗
PubMed2002

Neuronal involvement in the effect of an antisecretory factor-derived peptide on induced secretion in the porcine small intestine.

The antisecretory factor is a protein inhibiting enterotoxin-induced intestinal inflammation and hypersecretion. We studied the signaling pathway of three antisecretory factor-derived peptides (A1, A3 and A4) in the proximal and distal porcine small intestine. In vivo (ligated loops), only A3 significantly reduced the cholera toxin-induced fluid accumulation and only in proximal loops. A3 and A4 reduced Escherichia coli heat-labile enterotoxin-induced fluid accumulation in the proximal segment, whereas A1 and A3 reduced the Escherichia coli heat-labile enterotoxin-induced fluid accumulation in the distal segment. The secretory response to intraluminally added 5-hydroxytryptamine was not significantly inhibited by the peptides. The amount of intraluminal 5-hydroxytryptamine accumulated in cholera toxin-stimulated loops from the proximal segment was significantly reduced by A3. In vitro,the effect of A3 on secretagogue-induced increases in short-circuit current was recorded from proximal small intestine by the Ussing chamber technique. A3 decreased the tetrodotoxin sensitive effect of substance P. The in vivo results suggest that the antisecretory effect may involve inhibition of the local release of 5-hydroxytryptamine induced by cholera toxin, but not inhibition of secretory reflexes induced by 5-hydroxytryptamine. The in vitro results suggest that the effect of A3 lies beyond the surface epithelium, and involves mucosal neuronal structures.

Animals↗