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At least 595 records · Page 33Linked to original sources
PubMed2006

Ouabain-sensitive bicarbonate secretion and acid absorption by the marine teleost fish intestine play a role in osmoregulation.

The gulf toadfish (Opsanus beta) intestine secretes base mainly in the form of HCO3- via apical anion exchange to serve Cl- and water absorption for osmoregulatory purposes. Luminal HCO3- secretion rates measured by pH-stat techniques in Ussing chambers rely on oxidative energy metabolism and are highly temperature sensitive. At 25 degrees C under in vivo-like conditions, secretion rates averaged 0.45 micromol x cm(-2) x h(-1), of which 0.25 micromol x cm(-2) x h(-1) can be accounted for by hydration of endogenous CO2 partly catalyzed by carbonic anhydrase. Complete polarity of secretion of HCO3- and H+ arising from the CO2 hydration reaction is evident from equal rates of luminal HCO3- secretion via anion exchange and basolateral H+ extrusion. When basolateral H+ extrusion is partly inhibited by reduction of serosal pH, luminal HCO3- secretion is reduced. Basolateral H+ secretion occurs in exchange for Na+ via an ethylisopropylamiloride-insensitive mechanism and is ultimately fueled by the activity of the basolateral Na+-K+-ATPase. Fluid absorption by the toadfish intestine to oppose diffusive water loss to the concentrated marine environment is accompanied by a substantial basolateral H+ extrusion, intimately linking osmoregulation and acid-base balance.

Acids↗
PubMed1980

Vasoactive intestinal peptide secreting tumors of childhood.

A 2-year-old boy with failure to thrive, watery diarrhea, abdominal distention, hypokalemia, metabolic acidosis, and episodes of hypertension and sweating was found to have a calcified right lower quadrant mass. Blood levels of vasoactive intestinal peptide (VIP) and norepinephrine (NE) were elevated. Presurgical management with phenoxybenzamine hydrochloride and metyrosine was associated with an absence of expected postoperative hypotension, and resection of a benign ganglioneuroma resulted in prompt relief of all symptoms and return to normal of VIP and NE levels. Evidence supports the theory that VIP is the substance responsible for the diarrhea that accompanies some neural crest tumors.

Abdominal Neoplasms↗
PubMed1993

Cholera toxin-sensitive neurons in guinea pig submucosal plexus.

Cholera toxin (CT) increases intestinal secretions by direct stimulation of mucosal enterocytes; enteric neurons also may play a role. We tested the latter possibility by retrograde labeling of mucosal terminals in guinea pig small intestine with the B subunit of CT (B-CT) and by intracellular recordings from submucosal neurons during superfusion with CT. All vasoactive intestinal peptide (VIP)-positive neurons, and only VIP-positive neurons, were labeled with B-CT. Fluorogold (FG) was used to retrogradely label nerve terminals in submucosal arterioles in preparations in which B-CT labeled mucosal terminals; colocalization of B-CT with FG was observed in neurons up to 3 mm from the site of FG application. CT selectively depolarized neurons known to contain VIP. We conclude that all VIP-containing neurons, and only VIP neurons, in guinea pig submucosal plexus possess B-CT binding sites and can be activated by CT. Some of these neurons provide a dual innervation to both arterioles and mucosa. We suggest that one functional consequence of CT may be to activate vasodilator nerves, thus increasing vascular perfusion of the mucosa to further stimulate intestinal secretions.

Animals↗
PubMed1999

Pathogenic Escherichia coli increase Cl- secretion from intestinal epithelia by upregulating galanin-1 receptor expression.

Galanin is widely distributed in enteric nerve terminals lining the human gastrointestinal (GI) tract. We have shown previously that galanin-1 receptors (Gal1-R) are expressed by epithelial cells lining the human GI tract, and upon activation cause Cl- secretion. Because expression of this receptor is transcriptionally regulated by nuclear factor-kappa B (NF-kappa B), which is activated by enteric pathogens as a part of the host epithelial response to infection, we investigated whether such bacterial pathogens could directly increase Gal1-R expression in the T84-cell model system. Pathogenic Escherichia coli, but not nonpathogenic E. coli, activate a p50/p65 NF-kappa B complex that binds to oligonucleotides corresponding to a recognition site located within the 5' flanking region of the human GAL1R gene. Pathogenic E. coli, but not normal commensal organisms, increase Gal1-R mRNA synthesis and [(125)I]galanin binding sites. Whereas galanin increases short-circuit current (Isc) approximately 5-fold in uninfected T84 cells, exposure to pathogenic, but not nonpathogenic, E. coli results in galanin increasing Isc approximately 20-fold. To confirm the validity of these in vitro observations, we also studied C57BL/6J mice infected with enterohemorrhagic E. coli (EHEC) by gavage. Infection caused a progressive increase in both NF-kappa B activation and Gal1-R expression, with maximal levels of both observed 3 days after gavage. Ussing chamber studies revealed that colons infected with EHEC, but not those exposed to normal colonic flora, markedly increased Isc in response to galanin. These data indicate that pathogen-induced increases in Gal1-R expression by epithelial cells lining the colon may represent a novel unifying pathway responsible for at least a portion of the excessive fluid secretion observed during infectious diarrhea.

Animals↗
PubMed1977

Effect of propranolol on bile acid- and cholera enterotoxin-stimulated cAMP and secretion in rabbit intestine.

Stimulation of net secretion by deoxycholic acid (DCA) in the colon and by cholera enterotoxin (CE) in the jejunum is mediated by cAMP. Propranolol (Pr) inhibits adenylate cyclase (AC) activity and net secretion induced by bile acid in the colon. The aim of this study was to assess the organ specificity of DCA and CE as well as the selectivity of Pr inhibition. Three colonic and three jejunal loops were prepared in each of 8 rabbits treated intravenously with Pr, 4 mg per kg, 1/2 hr before loop construction and in each of 10 untreated control rabbits. One milliliter of DCA, 6 mM, CE, 10 mug per ml, or heat-inactivated CE or 0.9% NaCl, as basal controls were injected in random order into each of the loops. The volume of luminal fluid and mucosal AC were measured in each intestinal loop 5 hr later. DCA in the colon stimulated AC 2-fold (P less than 0.01) and luminal fluid 15-fold (P less than 0.01). CE in the jejunum stimulated AC 2.3-fold (P less than 0.01) and luminal fluid 9-fold (P less that 0.01). No significant effects on volume or AC occurred in response to CE in the colon or to DCA in the jejunum. Pr pretreatment completely prevented the stimulation of AC and luminal fluid by DCA in the colon but did not affect the action of CE in the jejunum of the same animals. Thus, DCA and CE are organ-specific stimulants of cAMP systems, and Pr is a selective inhibitor of certain inducers of cAMP and net secretion.

Adenylyl Cyclases↗
PubMed1986

Is the Golgi apparatus the obligatory final step for lipoprotein secretion by intestinal cells?

It is currently admitted that the synthesis and excretion of triglyceride-rich lipoproteins (chylomicrons and 'small chylomicrons') by intestinal epithelial cells involves the Golgi apparatus as an obligatory final step before exocytosis. The cells of the proximal intestine of the trout are an excellent model for investigating functional compartmentalization in the course of lipid absorption. Using this model, our data invalidate morphological data which were the basis for considering the Golgi apparatus as the mandatory final stage for their secretion. In particular, we show that triglyceride-rich particles can be transported directly from the endoplasmic reticulum to the intercellular space. Two pathways of intestinal lipoprotein excretion appear to coexist. One follows the classical export route, the second functions in a manner that bypasses the Golgi apparatus. The arguments used to affirm the requirement for the Golgi apparatus as a final step (glycosylation of apoprotein B, membrane vehicle for exocytosis) are discussed.

Animals↗
PubMed1977

The immunoglobulins of the turkey (Meleagris gallopavo). Isolation and characterization of IgG, IgM and IgA in body fluids, eggs and intraocular tissues.

The distribution of the immunoglobulins IgG, IgM, and IgA in turkey serum, bile, egg white, egg yolk, intestinal secretions, and some intraocular tissues has been studied. Just as in the chicken and the pigeon, IgG is the most abundant immunoglobulin in the serum and IgA in egg white, intestinal secretions and bile. In addition, IgM was detected in serum and egg white, and IgG in egg yolk, iris, vitreous body, and aqueous humor. The discussion deals with the importance of using purified immunoglobulin fractions and heavy-chain-specific antisera in disease studies in the turkey, specially in the case of infectious diseases which lead to the occurrence of "rheumatoid factors".

Animals↗
PubMed1981

Pathogenesis of acute bacterial diarrheal disorders.

Acute bacterial diarrheal disease is a worldwide problem of enormous magnitude. In recent years a number of bacteria have been added to the list of recognized etiologic agents causing acute diarrheal disease. This was made possible by our increased understanding of the mechanisms by which such bacteria cause diarrhea and by the development of methods to detect these bacterial enteropathogens. We are now able to define an etiologic agent in 50-80% of cases of acute diarrhea, depending on the particular population. The bacterial agents recently incriminated as important causes of diarrhea include E coli Y. enterocolitica, B. cereus, C. fetus, V. parahemolyticus, and many other coliform organisms. Establishment of an enteric infection depends upon a complex interplay between host defense mechanisms and bacterial virulence factors adapted to overcome these defenses. Bacterial enteropathogens cause diarrhea primarily by elaborating enterotoxins (which also requires the organisms to adhere to the surface of the intestinal cell) and by invading the intestinal mucosa. The number of known bacterial enterotoxins has rapidly increased. Enterotoxins cause intestinal secretion and diarrhea by stimulating the adenyl cyclase system or the guanyl cyclase system and by other mechanisms yet to be defined. The ability of enterotoxigenic bacteria to adhere to the intestine involves a specific binding interaction between bacterial structures called pili or fimbriae and specific receptors on the surface of intestinal cells. Both bacterial pili and the intestinal receptors are under genetic control. A variety of other bacteria, Salmonellae, Shigellae, Y. enterocolitica etc, must invade the mucosa to cause diarrheal disease. The ability to invade is essential to the pathogenesis of disease and requires particular surface characteristics of the bacterium as well as the active participation of both the bacterium and the host cell. The bacteria probably elaborate substances that signal the host cell to initiate the invasive process, i.e. endocytosis. The mechanism by which invasive bacteria evoke intestinal secretion is uncertain but is probably a multifactorial process involving products elaborated by the mucosal acute inflammatory reaction and enterotoxins elaborated by the bacteria.

Acute Disease↗
PubMed2006

Preliminary evaluation of the use of the sefA fimbrial gene to elicit immune response against Salmonella enterica serotype Enteritidis in chickens.

In the last 2 decades, the prevalence of Salmonella enterica serotype Enteritidis (Salmonella Enteritidis) has dramatically increased worldwide, becoming the leading cause of food-borne illnesses and an important public health issue. Many studies have suggested the role of the SEF14 fimbrial protein in the adhesion of Salmonella Enteritidis to the host. In the present study, the sefA gene, which encodes the main subunit of the SEF14 fimbrial protein, was cloned into a temperature-sensitive expression vector and transformed into a nonpathogenic, avirulent strain of Escherichia coli. The recombinant strain was used as a vaccine to elicit specific immune response against the SefA protein of Salmonella Enteritidis in 1-day-old chickens. The recombinant strain was reisolated from the intestines of treated birds for up to 21 days posttreatment, demonstrating its ability to colonize the intestinal tracts of 1-day-old chickens. In addition, immunoglobulin A (IgA) against the SefA protein was detected in intestinal secretions from treated birds at 7 days posttreatment and in bile samples from 14 to 21 days posttreatment by enzyme-linked immunosorbent assay. Nontreated birds did not show any evidence of intestinal colonization by the recombinant strain or anti-SefA IgA response in their bile or intestinal secretions. Preliminary evaluation of the recombinant strain showed a potential use of this strain to elicit protection against Salmonella Enteritidis infection in chickens. Further experiments are needed to study the ability of the recombinant strain to protect birds against Salmonella Enteritidis colonization.

Animals↗
PubMed1990

Enhanced local production of complement components in the small intestines of patients with Crohn's disease.

There is evidence that complement components may be formed locally in inflammatory lesions containing monocytes and macrophages. To investigate the role of complement in Crohn's disease we measured jejunal-fluid concentrations of the complement components C4, C3, and factor B by perfusion of a closed segment of the jejunum in 22 patients with Crohn's disease thought to be limited to the terminal ileum. The mean (+/- SEM) jejunal-fluid C4 concentration was 2.0 +/- 0.3 mg per liter, significantly higher than the mean level in 35 healthy controls (0.7 +/- 0.1 mg per liter; P less than 0.001). The mean C3 concentration was 1.0 +/- 0.1 mg per liter in the patients and 0.7 +/- 0.1 mg per liter in the controls (P less than 0.05). The factor B levels were similar in the two groups. Calculated rates of intestinal secretion of these components showed differences of the same magnitude. Leakage of protein from plasma was not increased. The jejunal-fluid:serum ratios of these complement proteins indicated that their appearance in the lumen of the jejunum was due to at least in part to local mucosal synthesis. The increased jejunal secretion of C4, but not C3 or factor B, paralleled the clinical activity of Crohn's disease. Values were normal in first-degree relatives of the patients (n = 13), patients with celiac disease (n = 8), and patients with ulcerative colitis (n = 4). We conclude that increased secretion of complement by clinically unaffected jejunal tissue in patients with Crohn's disease reflects the systemic nature of this disorder and may be due to the stimulated synthesis of complement by activated intestinal monocytes and macrophages.

Adolescent↗
PubMed1998

Levamisole inhibits intestinal Cl- secretion via basolateral K+ channel blockade.

BACKGROUND & AIMS: Phenylimidazothiazoles have recently been shown to activate wild-type and mutant cystic fibrosis transmembrane conductance regulator (CFTR) Cl- channels in transfected cells and were proposed as therapy for cystic fibrosis. The aim of this study was to investigate the effects of phenylimidazothiazoles on regulated transepithelial Cl- transport in intact epithelia. METHODS: T84 intestinal epithelial cells grown on permeable supports and stripped human colonic mucosal sheets were studied by conventional current-voltage clamping. Selective permeabilization of apical or basolateral membranes with the monovalent ionophore nystatin was used to isolate basolateral K+ and apical Cl- channel activity, respectively. 86Rb+ uptake was assessed for Na/K/2Cl cotransporter and Na+,K(+)-adenosine triphosphatase activity. RESULTS: In T84 monolayers and human colon, levamisole and its brominated derivative bromotetramisole failed to activate transepithelial secretion. In fact, these compounds dose-dependently inhibited secretory responses to the cyclic adenosine monophosphate agonist forskolin and the Ca2+ agonist carbachol. In permeabilized T84 monolayers, phenylimidazothiazoles weakly activated apical Cl- currents (consistent with their reported action on CFTR) and did not affect bumetanide-sensitive or bumetanide-insensitive 86+Rb+ uptake. Instead, they profoundly inhibited the basolateral Ba(2+)-sensitive and Ba(2+)-insensitive K+ currents. CONCLUSIONS: Phenylimidazothiazoles block K+ channels required for Cl(-)-secretory responses elicited by diverse pathways in model epithelia and native colon, an effect that outweighs their ability to activate apical Cl- channels.

Calcium↗
PubMed1982

Alpha 2-adrenoceptors inhibit the cholera-toxin-induced intestinal fluid accumulation.

The effects of adrenoceptor agonists and antagonists on the cholera-toxin-induced intestinal fluid accumulation and the mucosal levels of cAMP were investigated in vivo. Cholera toxin produced a marked fluid accumulation. Adrenaline inhibited the effect of the toxin in a dose-dependent manner. An alpha 2-adrenoceptor blocking agent yohimbine antagonized the effect of adrenaline. The alpha 1-adrenoceptor blocking agents prazosin and phenoxybenzamine failed to antagonize the effect of adrenaline. A high dose of a beta-adrenoceptor blocking agent pindolol did not antagonize the effect of adrenaline. Yohimbine or pindolol alone did not produce any effects on the toxin-induced fluid accumulation. However, prazosin and phenoxybenzamine per se inhibited the toxin-induced fluid accumulation. An alpha 2-selective agonist clonidine was slightly more potent than adrenaline, and was about 100-fold more potent than the alpha 1-selective agonist methoxamine in inhibiting the cholera-toxin-induced intestinal secretion. Clonidine, adrenaline and methoxamine failed to reduce the mucosal levels of cAMP, while these alpha-adrenoceptor agonists inhibited the toxin-induced fluid accumulation in the same preparations. These results suggest that the stimulation of alpha 2-adrenoceptors inhibit the cholera-toxin-induced intestinal secretion without reducing the whole mucosal levels of cAMP.

Adrenergic alpha-Agonists↗
PubMed1975

Transport of deutherium oxide across isolated rat small intestine.

1. Transport of deuterium oxide from a luminal perfusate containing 1% D2O was studied in Fisher & Gardners (1974) isolated preparation of perfused rat small intestine. 2. The kinetics of appearance of D2O in the intestinal secretion at the serosal surface fitted well to a single exponential function. 3. The steady-state concentration of D2O in this secretion was not significantly different from the concentration in the luminal perfusate. 4. The total tissue water contained D2O at a concentration, on average, 5% lower than that in the luminal perfusate. 5. There is no evidence to suggest discrimination in transport across the intestinal mucosa between H2O and D2O. 6. The kinetics of wash-in of D2O to intestinal secretion show that the ratio of flux out of the lumen to reflux back to the lumen is 1-38;1.

Animals↗
PubMed2002

Intestinal apolipoprotein B secretion is inhibited by the flavonoid quercetin: potential role of microsomal triglyceride transfer protein and diacylglycerol acyltransferase.

Recent studies have yielded evidence that plant flavonoids reduce hepatic lipid and apolipoprotein B (apoB) secretion. However, the possible role of flavonoids in regulating lipid and apoB secretion by the intestine has not been studied. The purpose of our study was to examine the effects of quercetin, a common dietary flavonoid, on TAG and apoB secretion in a human intestinal cell-line, CaCo-2. Differentiated postconfluent CaCo-2 cells grown on filters and pretreated with quercetin for 8 h were shown by ELISA to inhibit basolateral apoB secretion in a dose-dependent manner. At 15 microM, the secretion of both apoB-100 and apoB-48 were inhibited similarly. This effect was shown to be specific, as quercetin did not affect the incorporation of [35S]methionine/cysteine into secreted TCA-precipitable proteins. To determine the mechanism underlying this inhibitory effect, we examined two regulatory points: TAG availability and lipid transfer to the lipoprotein particle. Quercetin inhibited TAG synthesis under both basal and lipid-rich conditions, indicating that lipid availability is a determining factor in the regulation of apoB secretion by quercetin. The reduction was due at least in part to a decrease in diacylglycerol acyltransferase activity. We next examined lipid transfer or lipidation of the lipoprotein particle by analyzing microsomal TAG transfer protein (MTP) activity. Quercetin decreased MTP activity moderately. In summary, the data demonstrated that pharmacological concentrations of quercetin are a potent inhibitor of intestinal apoB secretion and that reduced lipid availability and lipidation in the lipoprotein assembly step are the mechanism for the suppression of apoB-containing lipoprotein secretion by quercetin in CaCo-2 cells.

Acyltransferases↗
PubMed1974

Binding of cholera toxin to mucins and inhibition by gastric mucin.

The effects of mucin on cholera toxin induced intestinal secretion was studied in the rat small intestine. Gastric mucin inhibited secretion when premixed with cholera toxin on an equal dry-weight basis. Neither salivary nor intestinal mucin inhibited the toxin's action in the intestine. Inhibition by gastric mucin was not reversed by a mucolytic agent or by hexoses or agents that bind hexoses. Plasma and serum did not inhibit the effects of cholera toxin in the intestine. Choleragen was labeled with (14)C and its binding to mucins and ganglioside was studied. Gastric mucin was shown to bind to choleragen, but less binding was observed when choleragen was dissociated into subunits by acid pH. Salivary and intestinal mucins bound intact choleragen but not the subunits at acid pH. Salivary mucin binding was reversed by N-acetyl neuraminic acid and neuraminidase. Ganglioside bound choleragen in both the intact and dissociated forms. Binding to the dissociated form was reversed by wheat germ agglutinin. Gastric mucin and ganglioside competed for binding to choleragen with the binding of intact choleragen greater for ganglioside and the affinity of the subunits greater for gastric mucin. Electrophoresis of labeled choleragen showed uniform labeling of the subunits dissociated by acid pH, but a major part of cholera toxin was found not to be labeled when fractionated with sodium dodecyl sulfate and 2-mercaptoethanol.

Animals↗
PubMed1994

Intestinal kinetics and dynamics of Escherichia coli heat-stabile enterotoxin in suckling mice.

The heat-stabile enterotoxin produced by Escherichia coli (ST) induces diarrhea by binding to receptors on intestinal cells, activating guanylyl cyclase, and increasing cyclic GMP. High- and low-affinity receptors for this toxin have been identified previously. ST induces intestinal secretion in suckling mice in picomole doses, suggesting a role for high-affinity receptors in this process. The present studies examine the relative roles of high- and low-affinity receptors in this process. The time course of changes in free ST concentrations in suckling mouse intestine was determined after intragastric inoculation. Also, binding characteristics of high- and low-affinity receptors and their coupling to guanylyl cyclase were defined in intestinal membranes from suckling mice. Intestinal concentrations of toxin and receptor binding characteristics empirically determined were used in a dynamic model correlating fractional occupancy of high- and low-affinity receptors with intestinal secretion to estimate their relative contributions to ST-induced diarrhea.

Animals↗