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At least 631 records · Page 35Linked to original sources
PubMed1988

Immune-related intestinal Cl- secretion. I. Effect of histamine on the T84 cell line.

The mast cell mediator, histamine, induces a rapid and transient increase in chloride secretion across monolayers of the human colonic epithelial cell line, T84. Threshold stimulation occurred at 3 X 10(-6) M histamine and a maximal effect at 10(-4) M. The effect was reproduced by the H1 agonists 2-methylhistamine and 2-pyridylethylamine, but not by the H2 agonists 4-methylhistamine and dimaprit, suggesting the involvement of an H1 receptor. Additionally, histamine's action was inhibited by an H1 antagonist, diphenhydramine, but not by an H2 antagonist, cimetidine. Histamine treatment increased free cytosolic calcium levels, but not those of adenosine 3',5'-cyclic monophosphate (cAMP) or guanosine 3',5'-cyclic monophosphate (cGMP). The mechanism of chloride secretion induced by histamine resembled that of carbachol, in that both 1) were associated with an increase in free cytosolic calcium, 2) had a site of activation at a basolaterally localized K+ channel, and 3) were potentiated by both cAMP- and cGMP-mediated secretagogues. These results suggest that histamine may act as an intestinal secretagogue via direct interactions with epithelial cells.

Biological Transport↗
PubMed1977

Interactions of intestinal lymph flow and secretion.

The relationship between lymph flow and intestinal secretion was studied in an isolated, vascularly perfused cat ileal preparation in which secretion was caused by three different means: 1) plasma dilution from a constant infusion of Tyrode solution (2.5 ml/min per kg), 2) elevation of intestinal venous pressure to 30 mmHg, and 3) exposure to cholera toxin. In the plasma-dilution group, lymph flow attained a peak value of 38 times control at 60-90 min following the onset of the infusion, after which time lymph flow progressively decreased. Concomitant to the rapid decrease in lymph flow was a rapid increase in intestinal secretion (filtration secretion). A similar pattern, i.e., a rapid increase in lymph flow followed by a progressive decrease in lymph flow and concomitant increase in filtration secretion, was observed in the venous hypertension group; however, peak lymph flow (20 X control) was observed within 10 min of the pertubation. No correlation between the onset of intestinal secretion and a decline in lymph flow was observed in the cholera toxin group.

Animals↗
PubMed2000

The effect of zaldaride maleate, an antidiarrheal compound, on acetylcholine-induced intestinal electrolyte secretion.

The effect of zaldaride on acetylcholine-induced colonic electrolyte secretion was examined. The short-circuit current response to acetylcholine was partially reduced by tetrodotoxin, a neuronal blocker, and was completely inhibited by atropine, an acetylcholine M receptor antagonist, in the rat colonic preparations. The tetrodotoxin sensitive effect was significantly inhibited by zaldaride, whereas the tetrodotoxin insensitive effect was not affected. Acetylcholine release from synaptosomes of submucosal nerves of guinea-pig colon was significantly reduced by zaldaride. Zaldaride may reduce colonic electrolyte secretion by acetylcholine due to the inhibition of acetylcholine release from synaptosomes of colonic submucosal nerves.

Acetylcholine↗
PubMed1976

Effect of caffeine on the human small intestine.

Methylxanthines produce intracellular accumulation of cyclic 3'5'-AMP (cAMP) by inhibition of phosphodiesterase and mucosal cAMP accumulation. Cyclic AMP is thought to mediate small intestinal secretion caused by some enterotoxins, hormones, and methylxanthines. These studies were designed to evaluate the effect of caffeine on small intestinal net fluid movement and transit times. The administration of caffeine in amounts ordinarily contained in many beverages and medications (75 to 300 mg) resulted in striking net secretion in the jejunum which lasted at least 15 minutes. This occurred in six of seven studies. Baseline net absorption of 0.5 ml per cm per hr was reversed to net secretion of 6.0 +/- 2.2 ml per cm per hr after oral caffeine ingestion (P less than 0.01). Net secretion also occurred in the ileum in seven of eight studies, but the onset of secretion appeared 35 min later than in the jejunum. These patterns of secretion correlated best with the passage of the intestinal bolus of caffeine rather than plasma caffeine levels. In contrast to other net secretory conditions, which increase the speed of transit, small intestinal transit times, as determined by dye dilution methods, were unchanged by caffeine. It is possible that methylxanthine-induced small intestinal secretion may play a role in the symptoms experienced by some patients with functional diarrhea.

Administration, Oral↗
PubMed1982

Humoral and cellular immunity in typhoid and paratyphoid carrier state, investigated by means of quantitative immunoelectrophoresis and in vitro stimulation of blood lymphocytes.

The humoral and cellular immunity of 8 Salmonella carriers and 9 non-carriers was investigated and compared to findings in normal persons. The antibody response in serum and intestinal secretions was investigated by means of crossed immunoelectrophoresis, and blood lymphocytes were investigated by in vitro stimulation. Both carriers and non-carriers showed increased levels of precipitating antibodies as well as lymphocyte responses, when compared to normal persons. No differences in the antibody responses either qualitatively or quantitatively were found between carriers and non-carriers. Only few precipitins could be detected in intestinal secretions. Lymphocyte responses to S. typhi and S. paratyphi were significantly higher in carriers and non-carriers than in the controls. No significant difference in lymphocyte response to S. typhi, S. paratyphi and mitogens was obtained between carriers and non-carriers. Thus, the carrier state seems not due to detectable major immunodeficiency.

Adult↗
PubMed1997

Protective immunity against Salmonella typhimurium elicited in mice by oral vaccination with phosphorylcholine encapsulated in poly(DL-lactide-co-glycolide) microspheres.

Encapsulation of vaccines in biodegradable microspheres provides excellent mucosal immunogens with a high potential for immunization against bacterial infections. We tested the protective immunity elicited by intragastric vaccination with phosphorylcholine (PC) encapsulated in poly(DL-lactide-co-glycolide) (DL-PLG) microspheres against Salmonella typhimurium in a mouse model of invasive intestinal infection. We chose PC as the antigen because it was found to elicit an immune response after intestinal exposure of mice to PC-bearing S. typhimurium and because anti-PC immunity protects mice against Streptococcus pneumoniae, another PC-bearing microorganism. Mice were primed intragastrically on days 1, 2, and 3 and boosted on days 28, 29, and 30 with PC (280 microg) coupled to porcine thyroglobulin (PC-thyr) encapsulated in DL-PLG microspheres, free PC-thyr, or blank microspheres. A significant rise in anti-PC immunoglobulin A (IgA) titers, as measured by an enzyme-linked immunosorbent assay, was observed in the intestinal secretions after immunization with PC-loaded microspheres, compared to the titers of mice immunized with free PC-thyr or blank microspheres. This antibody response peaked 14 days after the last boost and correlated with a highly significant resistance to oral challenge by S. typhimurium C5 (P < 10(-3)). Control mice were primed intraperitoneally on day 1 with 15 microg of PC in complete Freund's adjuvant and boosted on days 10, 14, and 20 with the same dose without adjuvant but via the same route. In these mice, the levels of anti-PC IgA in intestinal secretions were equivalent to those of the mice intragastrically immunized with PC-loaded microspheres, but protection was significantly weaker, suggesting that either the IgAs were not functional or that other immune mechanisms are important in protection. Taken together, our results highlight the potential of antigen encapsulation in DL-PLG microspheres for eliciting protective immunity against invasive intestinal bacterial diseases and suggest that a similar strategy could be used against diseases caused by other PC-bearing microorganisms.

Administration, Oral↗
PubMedDate not supplied

[Influence of classic enteropathogenic Escherichia coli on small bowel bacterial proliferation in infant's acute and persistent diarrhea].

UNLABELLED: Bacterial proliferation of the colonic microflora can occur in up to 50% of the infants with acute and persistent diarrhea. EPEC strains are frequently associated with bacterial proliferation in the small bowel lumen. The persistence of diarrhea might be due to the proliferation of EPEC in the intestinal lumen. PURPOSE: The present study was aimed at comparing the magnitude of the bacterial proliferation in the small bowel lumen in infants with acute and persistent diarrhea due to EPEC and other agents. PATIENTS AND METHODS: Fourty infants with diarrhea (23 with acute diarrhea and 17 with persistent diarrhea) underwent a naso-jejunal intubation for intestinal secretion culture of aerobes and anaerobes microorganisms. Stool samples were also collected for the investigation of enteropathogenic agents. RESULTS: Bacterial proliferation in the small bowel was detected in 32 (80%) infants; in 30 (75%) infants there was proliferation of aerobic microorganisms while in 17 (43%) infants there was proliferation of microorganisms belonging to the anaerobic microflora. There was no statistical difference in the bacterial proliferation between patients with acute and persistent diarrhea. In 16 patients EPEC strains were identified in the stool culture, and all of them showed bacterial overgrowth above 10(3) microorganisms/mL. In contrast in the 24 patients without EPEC in the stools only 16 (67%) showed bacterial overgrowth in the small bowel lumen (p < 0.01). The mean concentration of E. coli in the intestinal secretion was 8 x 10(5) microorganisms/mL among the patients with EPEC in the stools and 3 x 10(2) microorganisms/mL among the patients with no EPEC in the stools (p < 0.05). CONCLUSIONS: EPEC infection either acute or persistent induce favorable conditions for bacterial proliferation in the small bowel secretion in infants with diarrhea.

Acute Disease↗
PubMed1995

Electrophysiology of intestinal cholecystokinin secretion.

The control of gastrointestinal CCK secretion may occur at several points. A decrease in potassium conductance may depolarize the plasma membrane, activating calcium channels with a resultant stimulation in CCK release. The opposite may occur with increases in potassium conductance. The model presented in Fig. 8 suggests that the key control point in the understanding of CCK secretion is the regulation of L-type calcium channels. Whether a single second messenger pathway may regulate calcium channels stimulated by agents such as glucose, phenylalanine, bombesin and cAMP is an important area to pursue.

Adenosine Triphosphate↗
PubMed2000

Characterization of delta-opioid receptors and effect of enkephalins on IRD 98 rat epithelial intestinal cell line.

Using 3H-Tyr-D-Ala-Gly-Phe-D-Leu-OH (3H-DADLE) as a radioligand, delta-opioid binding sites on the IRD 98 rat epithelial cell line were identified. These sites were found to be reversible, saturable, specific and displayed high affinity for DADLE. Scatchard analysis revealed a dissociation constant (Kd) of 4.9+/-0.5 nmol/l, a maximum binding capacity (Bmax) of 1.7 pmol/mg protein, and 5x10(5) binding sites per cell. The presence of opioid receptors suggests the possibility that enkephalins directly control ion transport in enterocytes. In order to verify this hypothesis, investigations were designed to determine whether these receptors are functional and whether enkephalins can inhibit the stimulation of adenosine 3',5' cyclic monophosphate (cAMP) synthesis induced by cholera toxin. The increase in cAMP synthesis induced by cholera toxin was inhibited in a dose-dependent manner by H-Tyr-D-Ser-Gly-Phe-Leu-Thr-OH (DSLET), a delta-agonist. The enkephalinase inhibitor thiorphan potentiated this effect on IRD 98 cells, which contain enkephalinase. The action of DSLET was increased by 40% in the presence of this inhibitor. This effect was reversed by naltrindole, a potent delta-antagonist. Enkephalins can regulate intestinal secretion by acting directly on enterocytes: they thus have an antidiarrheal role, especially in the presence of an enkephalinase inhibitor.

Analgesics, Opioid↗
PubMed1969

Fecal neutral steroids and bile acids from germfree rats.

The amount and composition of fecal neutral sterols and bile acids excreted by adult male germfree and conventional rats have been determined. The amounts of neutral sterols excreted were 12.8 (germfree) and 19.5 (conventional) mg/kg of body wt per day. The germfree rats excreted cholesterol and lathosterol (methostenol was not assayed); the conventional rats excreted coprostanol and coprostanone in addition. The amounts of bile acids excreted were 11.3 (germfree) and 21.4 (conventional) mg/kg of body wt per day. The bile acids excreted by the rats were tentatively identified as tauro--muricholate, tauro-alpha-muricholate, and tauro-cholate, besides an unidentified component. The conventional rats excreted the corresponding unconjugated acids as well as many other unconjugated bile acids. No significant correlation was found between the amount of coprosterols and the total amount of neutral sterols excreted by the conventional rats. This suggests that bacterial reduction of cholesterol is not an important mechanism of increasing neutral sterol excretion of conventional rats as compared to germfree rats. Evidence is presented that suggests that this difference in neutral sterol excretion is due to changes in intestinal secretion and sloughing between the two types of animal. The factors reponsible for the differences in bile acid excretion have not been identified.

Animals↗
PubMed1983

Colonic cyclic AMP metabolism following chronic ethanol consumption in the rat: effect of hormonal secretagogues.

The colonic cyclic AMP system is known to be involved in intestinal secretion and can be stimulated by a variety of gastrointestinal hormones including prostaglandins. We have investigated the effect of chronic ethanol ingestion on the activity of the key enzymes in cyclic AMP metabolism--adenylate cyclase and cyclic AMP phosphodiesterase--in the colonic mucosa of the rat. Chronic ethanol consumption by feeding a nutritionally adequate liquid diet enhanced basal colonic adenylate cyclase activity significantly by 168% (p less than 0.01), but had no effect on colonic low Km cyclic AMP phosphodiesterase activity. In addition, various hormonal secretagogues were used to stimulate colonic adenylate cyclase. Colonic adenylate cyclase exhibited a significantly greater sensitivity and efficacy to prostaglandins and vasoactive intestinal peptide after chronic ethanol ingestion. Since increased intestinal cyclic AMP production due to an increased activity of intestinal adenylate cyclase is known to promote intestinal secretion of water and electrolytes, the frequently observed diarrhea in alcoholics may be explained at least in part by an enhanced production of colonic cyclic AMP.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1997

Phospholipase A2 secretion during intestinal graft ischemia.

The time-dependent appearance of phospholipase A2 (PLA2) activity in the preservation media of ischemic rat intestinal grafts is described. In controls, Ca2+-dependent, secretory PLA2 activity accumulated rapidly during the first 6 hr of ischemia, followed by a linear increase for up to 48 hr. LDH levels, by contrast, increased linearly throughout the 48 hr of ischemia. Addition of inhibitors of PLA2, cyclooxygenase, and lipooxygenase blocked accumulation of PLA2, but not LDH. PX-13, a novel PLA2 inhibitor, was most effective: 40 microM inhibited release by 86%, while 25 microM indomethacin (cyclooxygenase blocker) or nordihydroguiaretic acid (lipooxygenase blocker) inhibited 41 and 36%, respectively. That appearance of PLA2 activity, but not LDH, is attenuated by inhibitors of the eicosanoid cascade suggests a secretory event rather than leakage from dying cells. The secreted PLA2 is most likely the proinflammatory sPLA2 that has been implicated as a stress-induced protein and priming agent in ischemia-reperfusion injury.

Alkanesulfonates↗
PubMed1989

Influence of a glycine or proline substitution on the functional properties of a 14-amino-acid analog of Escherichia coli heat-stable enterotoxin.

Analogs of Escherichia coli heat-stable enterotoxin (ST) differing in chain length or the presence of turn-forming residues were assessed for binding to receptors, activation of particulate guanylate cyclase, and stimulation of secretion in suckling mice. These analogs included the native 18-amino-acid peptide (ST), the 14-amino-acid carboxy terminus of this native peptide with a proline at position 12 (ST[5-18]proline), and the 14-amino-acid carboxy terminus in which the proline at position 12 was substituted with glycine (ST[5-18]glycine). Each analog bound to the receptor in a dose-dependent fashion, completely displacing [125I]ST in competitive binding assays. However, their potencies differed significantly: ST demonstrated the highest affinity (inhibition constant [Ki], 10(-9) M), followed by ST[5-18]proline (Ki, 10(-7) M) and ST[5-18]glycine (Ki, 10(-6) M). Similarly, these peptides maximally activated particulate guanylate cyclase and stimulated intestinal secretion in suckling mice. Their rank order of potency in these assays was similar to that described for receptor binding: ST greater than ST[5-18]proline greater than ST[5-18]glycine. These data demonstrate that the full peptide structure is not absolutely required for pharmacological, biochemical, or biological activity. However, the four amino-terminal residues contribute significantly to the potency of these peptides. In addition, the turn imposed by the proline residue at position 12 is not absolutely required for receptor occupancy or activation of the biochemical cascade that results in intestinal secretion. However, it significantly increases the potency of the toxin. These data illustrate the importance of primary and secondary structures to the biochemical, pharmacological, and physiological activities of the ST produced by E. coli.

Amino Acid Sequence↗
PubMed2002

Transmural pressure induces IL-6 secretion by intestinal epithelial cells.

Although intestinal epithelial cells (IECs) are known as an important source for IL-6, it is not known whether mechanical forces affect IL-6 production. We investigated how transmural pressure modulates IL-6 synthesis and activation of transcription factors in IECs. Pressure was loaded onto IEC-18 cells by introducing compressed helium gas into the cell culture flask for 1-48 h. IL-6 release into the culture media was determined by cell proliferation bioassay using an IL-6-dependent mouse hybridoma cell line (7TD1). Exposure to pressure (80 mmHg) significantly enhanced IL-6 release into the culture media from IEC-18 cells at 12 h. Under control conditions, IL-6 secretion was directed to the basolateral side, but after exposure to pressure IL-6 secretion was increased in both the apical and basolateral sides. A nuclear factor kappa B (NF-kappaB) decoy reversed completely the pressure-induced increase of IL-6 secretion by IEC-18 cells. Pressure treatment enhanced IL-6 mRNA expression in IECs within 6 h. Pressure loading significantly enhanced the activation of both NF-kappaB and NF-IL-6 from 1h in the nuclear protein of IEC-18 cells as assessed by the electrophoretic mobility shift assay using FITC-conjugated specific primers. Increased phosphorylation of I-kappa B was also demonstrated in the cytosol of IEC cells within 1h by Western blot analysis. These results suggest a possible role for pressure loading in immune modulation of the intestinal mucosa by the stimulation of IL-6 release from intestinal epithelial cells.

Animals↗
PubMed1992

Local and systemic antibody response in Balb/c mice immunized with Entamoeba histolytica trophozoites.

Several immunization schedules with E. histolytica trophozoites were tested on Balb/c mice in order to induce antibody responses, both in intestinal secretions and in serum. Mice were immunized either orally, systemically, or using one of two combined schedules: the oral route followed by the systemic route (footpad), or vice versa. Each of the immunization schedules used in this project induced an anti-E. histolytica antibody response and there appears to be a correlation between the immunization route employed and the immunoglobulin isotype induced in the gut. Secretory IgA production is favored by the oral administration of trophozoites, whereas mucosal IgG appears to be enhanced by the systemic immunization route. Both schedules are effective in the induction of secretory IgA in the gut, yet higher and earlier levels of IgA appear in orally immunized mice. When systemic immunization is employed, the increase in antibody levels in the intestinal fluid is slower, and IgG is the predominant class. The combined oral/systemic routes of immunization appear to be comparably effective for the induction of local and systemic IgA and IgM antibody production. However, mice immunized first systemically and then locally produce more IgG in both compartments. Combined schedules modify the isotype pattern of antibody responses in serum and in intestinal secretions when compared with single (i.e., oral or systemic) schedules, but they do not appear to favor a secretory IgA immune response.

Administration, Oral↗
PubMed1981

Factors affecting iron balance.

The availability of radioisotopes of iron led to the performance of physiologic studies of the absorption, excretion, and kinetics of iron. The effects of dietary constituents and intestinal secretions upon iron absorption have been thoroughly explored and have permitted the development of tools for nutritional studies in various geographic areas of the world. The basic mechanisms for regulation of iron absorption are not fully understood. However, the isolation and characterization of newer iron-binding proteins, the existence of mucosal receptors in which there is competition for iron-binding sites with other metals, and the identification of a number of animal models with genetic abnormalities of iron absorption provide promise for development in the foreseeable future. The means by which the body informs the intestine to increase or decrease iron absorption is poorly understood, and the abnormality in hemochromatosis and iron overloading disorders remains unexplained. Much has been learned in recent years regarding the structure of iron-containing proteins and the variations that exist in different species. Similar problems remain to be solved with regard to the intermediary metabolism of iron in red blood cell precursors and other cells in the body. It is postulated that the combined usage of physiologic, biochemical, and immunologic investigations will provide the basic information required.

Absorption↗