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PubMed2002

Secreted intestinal surfactant-like particles interact with cell membranes and extracellular matrix proteins in rats.

Surfactant-like particles (SLP) are secreted from enterocytes basolaterally into the lamina propria, and reach the apical surface through the intercellular tight junctions. Interactions of SLP with apical and basolateral membranes and with extracellular matrix proteins were measured using a solid-phase binding assay and gel overlays. Small-intestinal SLP bound to basolateral membranes much more than to apical membranes, and more tightly to fibronectin than to laminin (affinity constant K(a) = 1.23 x 10(-2) microg vs. 0.67 x 10(-2) microg; maximal number of binding sites 4.1 microg x ml(-1) vs. 0.32 microg x ml(-1)), but did not bind to collagen types I or IV. Small-intestinal SLP bound fibronectin more than colonic or gastric SLP. Binding to fibronectin was inhibited only partially by RGD peptide and gelatin, but not by heparin. An antibody against alpha(v) integrin also identified the fibronectin-binding component in SLP at approximately 220 kDa, which is the expected size for integrin heterodimers. SLP binding to apical microvillous membranes was weaker and was inhibited by heparin. SLP bound more strongly to heparin itself, and this binding was inhibited by glucuronic acid and chondroitin sulfate. These data are consistent with the hypothesis that the time spent by secreted SLP in the lamina propria is prolonged by strong interactions with proteins in the basolateral membranes, and in the intestinal lumen by weaker interactions with apical membrane components, including heparin. These interactions may allow SLP the time to exert their functions in each tissue compartment.

Animals↗
PubMed1991

Mechanism of intestinal secretion. Effect of serotonin on rabbit ileal crypt and villus cells.

To determine the mechanism of action of an intestinal secretagogue, serotonin, we have isolated crypt and villus cells and demonstrated Na:H and Cl:HCO3 exchange activity using the intracellular pH-sensitive fluorescent dye, 2,7-bis (carboxy-ethyl)-5,6-carboxy-fluorescein. Serotonin alkalinized both crypt and villus cells. Alkalinization in villus cells was HCO3 dependent and Na independent. In contrast, alkalinization in crypt cells was HCO3 independent and Na dependent. In villus cells, recovery from an alkaline load induced by Cl removal, 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid or propionate pulse, known to occur via the Cl:HCO3 exchange, is inhibited by serotonin. In contrast, in crypt cells, recovery from an acid load induced by Na removal, amiloride and NH4Cl pulse, known to occur via Na:H exchange, is stimulated by serotonin. These data suggest that serotonin is inhibiting Cl:HCO3 exchange in villus cells and stimulating Na:H exchange in crypt cells. These effects of serotonin would be expected to inhibit coupled Na and Cl absorption by villus cells and stimulate HCO3 secretion by crypt cells in the intact ileum.

Animals↗
PubMedDate not supplied

Enhancement of sodium intestinal secretion in relation to absorption in malnourished rats. Hyperosmolar challenge.

Two experimental models were tried in young malnourished rats in order to study effect of an hyperosmolar challenge in the small intestine on the bi-directional fluxes of sodium. Weanling rats were fed with energy restricted diets. In model I 1 mL of NaCl 900 mOsm/kg was introduced in the small intestine of the rats and left from 5 up to 70 min, in order to determine the moment of higher net Na+ secretion, which occurred at 10 min. In model II, the bi-directional fluxes of Na+ and Cl- were studied using NaCl or mannitol 900 mOsm/kg under the effect of mecholil, atropine or 2-4 dinitrophenol, for 10 min. Mecholil decreased the Na+ absorption enhancing the net secretion. Control rats were used as reference. In the restricted diets animals occurred an increase of the net secretion stimulated by NaCl 900 mOsm/kg, and this effect was enhanced by mecholil. It is suggested that in malnutrition there is an impairment in Na- intestinal absorption.

Animals↗
PubMed1995

Inhibition of intestinal secretion by rice.

Rates of stool output are reduced when cooked rice is incorporated into oral rehydration solutions. We found that a fraction extracted from rice inhibited the response of intestinal epithelial crypt cells to adenosine 3'5'-cyclic monophosphate, a major intracellular mediator of secretion. This response to rice was seen as an inhibition of cell shrinkage and of chloride efflux in fresh suspended guinea pig crypt cells. The active fraction was of low molecular weight (< 1.5 kDa), hydrophobic, and not a peptide or glycoprotein. It may be chloride-channel blocker.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1978

Intestinal secretion of sulphanilic acid by the isolated mucosa of guinea pig jejunum.

Tissue uptake and transepithelial permeation of 35S-sulphanilic acid were studied in the isolated guinea pig jejunal mucosa. Methoxy-3H-inulin added simultaneously served as a marker for the extracellular space and permeability of paracellular shunt pathways in the preparation. The uptake of sulphanilic acid from the blood side exceeded that from the luminal side 4--7 fold. The permeation of the acid was strongly correlated to the permeation of inulin. At 5 micrometer and 2.5 mM sulphanilic acid under aerobic conditions, the regression lines for the permeation from lumen to blood pass almost through the origin, while the regression lines for the permeation from blood to lumen intersect the ordinate at a positive Y-value. In anaerobiosis, at 25 mM sulphanilic acid, or with addition of p-toluene sulphonic acid only one regression line is obtained for the permeation in both directions. It is concluded that besides a permeation of sulphanilic acid across inulinpermeable shunt pathways an active transport system exists, which transfers the acid from the blood to the luminal side. This system is saturable, depends on aerobic energy and exhibits mutual inhibition by a structurally related compound. The results are comparable to those previously obtained with cardiac glycosides and quaternary ammonium compounds, in the same preparation. Thus, the intestinal mucosa is able to secrete the same classes of compounds which are secreted by the liver and the kidney.

Aerobiosis↗
PubMed1980

Intestinal secretion of lipids and lipoproteins during carbohydrate absorption in the rat.

To assess the effects of carbohydrate ingestion on the characteristics and quantities of triglyceride-rich lipoproteins produced by the intestine, mesenteric lymph was collected from rats receiving intraduodenal infusions of saline, sucrose or starch. Lymph total lipid (mg/hour) was greatest during saline infusion, decreased during sucrose and became significantly less (P less than 0.05) during starch infusion. Lipoproteins were isolated from lymph by ultracentrifugation followed by gel filtration chromatography. During saline infusion total lipid in very low density lipoproteins (VLDL) was 2-fold higher than total lipid in chylomicrons; with both carbohydrate infusions this ratio increased to seven. Both carbohydrates significantly lowered the rate of secretion of total lipid as chylomicrons. The VLDL lipid secretion rates during sucrose infusion were equivalent to those during saline, whereas starch infusion tended to decrease VLDL lipid secretion rates. These results suggest that during the process of carbohydrate absorption, carbohydrate does not enhance the flow of intestinal VLDL into the circulation; digestion and absorption of complex carbohydrates in fact may retard the intestinal contribution of triglyceride-rich lipoproteins.

Animals↗
PubMed1974

Experimental Cholera in Chinchillas: the Immune Response in Serum and Intestinal Secretions to Vibrio cholerae and Cholera Toxin.

The immune response to Vibrio cholerae and cholera toxin was studied in chinchillas inoculated intra-intestinally with 10(8) viable V. cholerae 596B. Sera and intestinal fluids were collected from animals on days 1, 2, 3, 5, 7, 10, 14, 30, and 60 postinoculation, and antibodies were quantified by various methods. When radiovibriolytic and radiotoxin precipitin tests were used, a significant (fourfold) rise in both antibacterial and antitoxic titers was detected in intestinal fluids on the 2nd day of infection. In contrast, a significant rise in serum antibodies occurred between days 3 and 5. Since the acute phase of the chinchilla disease lasts 1 to 3 days, recovery coincided with rise in intestinal antibody but not with rise in serum antibody. Our results indicate that both antibacterial and antitoxic mechanisms are operative in chinchilla cholera and that the initial and crucial immune response is local in nature.

Journal Article↗
PubMed2000

Weaning induces an increase in the number of specific cytokine-secreting intestinal lymphocytes in mice.

Intestinal immunity differs from systemic immunity in several aspects and is frequently studied separately. In this work we have analysed the frequency of mononuclear cells spontaneously secreting the cytokines IL-2, IL-4, IL-5, IL-6, IL-10, interferon gamma (IFN-gamma) and tumour necrosis factor (TNF-alpha), in Peyer's patches and lamina propria of small intestine in mice by enzyme linked immunosorbent spot (ELISPOT) during 1 month after weaning. We have found a high percentage of spontaneous Th(1)as well as Th(2)cytokine-secreting lymphocytes in both populations, Peyer's patches and lamina propria. An increase in the number of the lymphocytes secreting most of the studied cytokines, at 1 and 2 weeks after weaning, was also observed. These results suggest that the increase in the number of cytokine secreting lymphocytes may be one of the potential mechanisms involved in the development of the intestinal immune system at weaning.

Animals↗
PubMed1994

Active intestinal secretion of the fluoroquinolone antibacterials ciprofloxacin, norfloxacin and pefloxacin; a common secretory pathway?

The transepithelial transport of three fluoroquinolones, norfloxacin, ciprofloxacin and pefloxacin has been compared by using cultured human intestinal Caco-2 cell-layers. Absorptive (apical-basal) fluxes of ciprofloxacin and norfloxacin are small relative to basal to apical fluxes. Norfloxacin and ciprofloxacin are thus subject to active transepithelial secretion. Active net secretion of norfloxacin displays saturation kinetics with Vmax and Km values of 36.2 +/- 6.9 nmol.cm-2.hr-1 and 1.42 +/- 0.79 mM. In contrast, transepithelial pefloxacin fluxes are large, show marked saturation while the direction of net flux is variable and small relative to transepithelial fluxes. Norfloxacin, pefloxacin and ciprofloxacin are all subject to accumulative transport across the basal surface of Caco-2 cell layers. A number of 4-quinolones and fluoroquinolones are capable of inhibition of both net secretion of ciprofloxacin and cellular accumulation across the basal-lateral cell surface. Cinoxacin, a 4-quinolone may selectively inhibit exit from the cell across the apical membrane. Cross-competition studies suggest that fluoroquinolones may compete for a common carrier at the basal-lateral membrane. It is likely that the mechanism of transepithelial secretion involves a common accumulative transport at the basal-lateral membrane followed by facilitated exist across the apical membrane. Pefloxacin may interact with a brush-border carrier for which norfloxacin and ciprofloxacin are poor substrates, enhancing the absorptive flux of this fluoroquinolone.

Biological Transport↗
PubMed1998

Crucial role for 5-HT in cholera toxin but not Escherichia coli heat-labile enterotoxin-intestinal secretion in rats.

BACKGROUND & AIMS: Many consider cholera toxin (CT) and Escherichia coli heat-labile enterotoxin (LT) to be functionally identical. Both increase intracellular adenosine 3',5'-cyclic monophosphate concentration; however, differences between the two and the severity of the diseases they cause have been reported. The secretagogue 5-hydroxytryptamine (5-HT) is implicated in CT-induced secretion, but its role in LT-induced secretion is unclear. We tested the hypothesis that LT fails to recruit 5-HT in its secretory processes. METHODS: In vivo small intestinal perfusions were undertaken in adult male Wistar rats after incubation with equipotent doses of CT or LT, or saline. Small intestinal 5-HT release and the effect on net small intestinal water and electrolyte transport of (1) pharmacological depletion of 5-HT; (2) blockade of 5-HT type 2, 3, and 4 receptors; and (3) pretreatment with lidocaine, hexamethonium, and atropine were determined. RESULTS: CT- but not LT-induced secretion was accompanied by 5-HT release, reduced by 5-HT depletion, and inhibited by each 5-HT antagonist. By contrast, lidocaine and hexamethonium inhibited secretion induced by both toxins. CONCLUSIONS: LT induces secretion without recruiting a 5-HT-dependent cascade. This may account for differences in clinical severity of the diseases CT and LT cause and has implications for the development of antisecretory therapies.

Animals↗
PubMed1988

Adrenal and intestinal secretion of catecholamines and neuropeptides during splanchnic artery occlusion shock.

Plasma levels of catecholamines and neuropeptides (met-enkephalin, ME; neurotensin, NT; neuropeptide Y, NPY; peptide YY, PYY; vasoactive intestinal polypeptide, VIP; cholecystokinin, CCK; bombesin, BMB) were examined in the femoral artery (FA), adrenal vein (AD), and portal vein (PV), in eight cats under halothane anesthesia at baseline (S1), at the end of a 2-hr ligation period of the major splanchnic arteries (celiac trunk, superior and inferior mesenteric arteries) (S2), immediately (S3) and 30 min (S4) after splanchnic reperfusion, and after the administration of naloxone (1 mg/kg, i.v.) (S5). During S2, there was a significant increase in portal vein VIP levels, while the other variables (hemodynamics, hormone levels) remained unchanged. During early shock (S3), significant (10- to 30-fold) increases in adrenal secretion of all catecholamines, ME, NT, NPY, and PYY occurred, while VIP and PYY were significantly released into the PV, and two- to tenfold increases in femoral artery catecholamine and ME levels were observed. Later shock (S4) led to a further fivefold increase, compared to S3, in adrenal release of norepinephrine (NE), dopamine (DA), and ME. Following naloxone administration (S5), the adrenal medullary release of NE, epinephrine (EPI), DA, NT, and NPY was significantly (twofold) increased; however, the animals' hemodynamic situation did not improve.

Adrenal Glands↗
PubMed1992

Calcium-calmodulin-dependent activation of adenylate cyclase in prostaglandin-induced electrically-monitored intestinal secretion in the rat.

The calcium-calmodulin antagonist 5-iodo-C8-W7 inhibited the PGE2-induced stimulation of cAMP production by isolated enterocytes from rat small intestine. It also reduced the secretory response of intestinal sheets to PGE2, measured as a rise in short-circuit current. It did not however, inhibit the electrical responses to forskolin and dibutyryl cAMP, nor to acetylcholine, a secretagogue whose effect is not mediated by cAMP. It is concluded that the receptor-mediated activation of adenylate cyclase and the subsequent secretory response are dependent upon calcium-calmodulin.

Acetylcholine↗