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At least 919 records · Page 51Linked to original sources
PubMed2003

Modulation of gut physiology through enteric toxins.

Diarrheal diseases caused by microorganisms and their toxins are a major cause of mortality and morbidity throughout the world. Acute diarrhea is mainly caused due to increased intestinal secretion, commonly as a result of infection with enterotoxin producing organisms (enterotoxigenic Escherichia coli, Vibrio cholera) or due to decreased intestinal absorption from infection with organisms that damage the intestinal epithelium (enteropathogenic E. coli sp., Shigella sp., Salmonella sp.) The studies of the impact of enteric pathogens and their virulence factors exert their effect by producing toxins, called bacterial toxins. The protein toxins are produced by diverse group of bacteria. Most of the bacterial toxins exert their effect through involvement of ADP-ribosylation proteins; otherwise essential for several cellular functions while other toxins involve guanylate cyclase systems or calcium and protein kinases for their ultimate action.

Animals↗
PubMed2000

Novel targets for the pharmacotherapy of diarrhoea: a view for the millennium.

Acute diarrhoea continues to carry a high morbidity and mortality worldwide. Intestinal infection is the major cause of acute diarrhoea although the prevalence of individual pathogens varies according to geographic location. In many countries in the industrialized world, reports of intestinal infections continue to increase; these are largely related to waterborne and foodborne outbreaks. Acute diarrhoea may be due to increased intestinal secretion, commonly as a result of infection with enterotoxin-producing organisms (enterotoxigenic Escherichia coli, Vibrio cholerae) or to decreased intestinal absorption from infection with organisms that damage the intestinal epithelium (enteropathogenic E. coli, Shigella sp., Salmonella sp.). Although oral rehydration therapy has reduced the mortality associated with acute diarrhoea, the diarrhoea attack rate remains unchanged and stool volume often increases during the rehydration process. The search for agents that will directly inhibit intestinal secretory mechanisms and thereby reduce stool volume has been going on for more than 20 years. Research during the past decade has highlighted the importance of neurohumoral mechanisms in the pathogenesis of diarrhoea, notably the role of 5-hydroxytryptamine, substance P, vasoactive intestinal polypeptide and neural reflexes within the enteric nervous system. Cholera toxin, E. coli enterotoxins and Clostridium difficile toxin A are known to invoke these mechanisms in diarrhoea pathogenesis. This new dimension of intestinal pathophysiology has already exposed possible novel targets for anti-secretory therapy, namely, 5-HT receptor antagonists, substance P antagonists and the possibility for potentiating the proabsorptive effects of endogenous enkephalins by use of enkephalinase inhibitors. There now seems to be a real possibility that anti-secretory therapy will become more widely available in the future.

Animals↗
PubMed1986

Electrical measurement of chloride secretion in the perfused human jejunum: effects of theophylline and prostaglandin E1.

The effects of intraluminal theophylline or prostaglandin E1 (PGE1) on transepithelial potential difference (PD) were examined in the human jejunum in vivo with a quadruple lumen perfusion tube. To measure transepithelial PDs, we placed one of the Ag/AgCl electrodes in the jejunal lumen and the other in the subcutaneous region of the left forearm of the subjects. Infusion of theophylline or PGE1 into the jejunal lumen produced a change in the PD, the lumen being more negatively charged. The magnitude of the change in PD for 2.4 X 10(-3) M theophylline was 3.3 +/- 0.48 mV (mean +/- S.E., n = 6) and that for 10(-6) M PGE1 was 5.0 +/- 0.60 mV (n = 6). In addition, the change in the PD induced by simultaneous infusion of both 2.4 X 10(-3) M theophylline and 10(-7) M PGE1 was about twice as large as the sum of those induced by individual infusion of the same concentration of theophylline or PGE1. We concluded that these PD changes occurred primarily by stimulation of electrogenic Cl secretion in the jejunum. Further exploitation of this method to determine PD might be useful for clinical investigation of the intestinal secretion.

Adult↗
PubMed2001

[Effect of rhubarb on intestinal immune associated secretion in healthy mice and in burn mice].

OBJECTIVE: To explore the therapeutic mechanism of rhubarb (sennosides) in protecting intestinal muco-membranous barrier by observing the change of intestinal immune associated secretion (IIAS) in mice before and after burn and the enhancing effect of rhubarb on it in healthy and in burn mice. METHODS: Bal b/c mice were divided into 4 groups. Group A (n = 8), untreated healthy mice; Group B (n = 11), healthy mice treated with 10% rhubarb decoction 12 ml/kg, once every 6 hrs; Group C (n = 7), the mice with 30% back full-thickness burn and no treatment was given; Group D (n = 9), the mice with 30% back full-thickness burn and treated with 10% rhubarb decoction 12 ml/kg, once every 6 hrs. The animals were killed 24 hrs after burn, the intestinal juice was collected after intestinal lavage, and centrifuged for determination of IgA, total protein, C3 and high density lipoprotein. RESULTS: IgA content in intestinal juice of Group A, B, C and D were 93.5 +/- 13.7 mg/L, 150.8 +/- 44.6 mg/L, 43.4 +/- 21.5 mg/L and 59.8 +/- 19.3 mg/L respectively, suggesting that it was significantly reduced by burn (P < 0.05), while rhubarb decoction could increase it in either healthy or burn mice (P < 0.05). The other immune associated substance, such as total protein, C3 and high density lipoprotein in intestinal juice were also increased significantly after rhubarb decoction treatment. CONCLUSION: Rhubarb could increase the reduced intestinal juice IgA content in mice caused by burn, it may be an important mechanism of rhubarb in protecting muco-membranous barrier.

Adjuvants, Immunologic↗
PubMed1980

Effect of VIP infusion in water and ion transport in the human jejunum.

Infusion of vasoactive intestinal polypeptide (VIP) is known to cause intestinal secretion in animal models. The present study was designed to answer the question whether VIP has a similar effect on the human intestine. Pure porcine VIP was administered by constant i.v. infusion to healthy subjects while their jejunum was perfused with a plasma-like electrolyte solution. At the lowest VIP infusion rate (100 pmol/kg/hr), plasma VIP levels rose two- to four-fold, and there was an increase in the transmucosal potential difference but no change in sodium chloride absorption. At higher VIP infusion rates (200 and 400 pmol/kg/hr), VIP plasma concentrations rose to levels commonly observed in patients with pancreatic cholera syndrome. At these levels VIP caused a dose-dependent decrease of water and sodium absorption. Chloride absorption changed to secretion, while bicarbonate movement remained completely unaffected. Chloride secretion was active, since it occurred against an electrical and chemical gradient. All changes induced by VIP were reversible after discontinuance of VIP infusion. Our observations suggest that elevated levels of circulating VIP are capable of affecting water and ion movement in the human jejunum. They lend support to the hypothesis that high levels of circulating VIP may be a mediator of secretory diarrhea in some patients with pancreatic cholera syndrome.

Adult↗
PubMed1978

The effect of adsorbant and anti-inflammatory drugs on secretion in ligated segments of pig intestine infected with Escherichia coli.

Four adsorbant drug preparations, Kaopectate, colloidal Attapulgite, noncolloidal Attapulgite and Pepto-bismol were investigated for their effects on fluid accumulation in ligated segments of pig intestine inoculated with enteropathogenic Escherichia coli. Two anti-inflammatory drugs. aspirin and methylprednisolone, and two antibiotics, lincomycin and polymyxin B, were also tested. All the drugs except the two anti-inflammatory products were given by injection into the lumen of the intestine. Aspirin was given orally and methylprednisolone was given intramuscularly. The antibiotics were tested at levels at which they had no significant antibacterial effect in in vitro tests. The adsorbant drugs colloidal Attapulgite and Pepto-bismol were shown to be effective in reducing fluid accumulation in ligated segments of pig intestine infected with enteropathogenic E. coli. In the case of Peptobismol this effect was associated with an antibacterial effect as well as an antitoxic effect, probably due to its adsorbant properties. It is possible that an aspirin-like effect in the gut due to the active ingredient bismuth subsalicylate may have contributed to the effectiveness of Pepto-bismol. Colloidal Attapulgite was demonstrated to have an antitoxic effect but did not have an antibacterial effect. In high doses, the anti-inflammatory drugs acetylsalicylic acid and methylprednisolone were marginally effective in reduction of fluid accumulation in the same test system. Lincomycin was shown to reduce intestinal fluid secretion, whereas polymyxin B had no effect.

Animals↗
PubMed2004

Function of opioids in the enteric nervous system.

Alterations in gastrointestinal motility and secretion underlie the constipating action of therapeutically administered opiates. The prototype opiate is morphine, which acts to delay gastric emptying and intestinal transit, to suppress intestinal secretion of water and electrolytes and to suppress transport of bile into the duodenum. The effects of opiates, synthetic opioids and endogenously released opioid peptides on these organ-level gastrointestinal functions reflect actions on electrical and synaptic behaviour of neurones in the enteric nervous system. Adverse effects and positive therapeutic effects of administration of opioid-receptor-blocking drugs on the digestive tract must be understood in the context of the neurophysiology of the enteric nervous system and mechanisms of neural control of gastrointestinal smooth muscle, secretory glands and blood-lymphatic vasculature. We review here the integrated systems of physiology and cellular neurobiology that are basic to understanding the actions of opioid agonists and antagonists in the digestive tract.

Animals↗
PubMed1987

Influence of gastrointestinal peptides on bile acid transport by isolated rat hepatocytes.

While numerous effects of gut peptides on gastric, pancreatic, and intestinal secretion have been described, there has been little investigation of the influence of these peptides on hepatic function. In the present studies, effects of vasoactive intestinal peptide (VIP), somatostatin, thyrotropin-releasing hormone (TRH), and bombesin on taurocholate transport by isolated rat hepatocytes have been examined. Somatostatin, TRH, and bombesin in incubation media produced no change from control incubations with regard to either uptake of taurocholate by hepatocytes or efflux of bile acid from preloaded cells. However, incubation of hepatocytes with VIP produced a significant decrease in taurocholate uptake (1.34 +/- 0.13 versus 1.73 +/- 0.16 nmole.min-1.10(6) cells-1, P less than 0.001). Studies with verapamil, a calcium-channel blocking agent, and theophylline, an inhibitor of cAMP catabolism, failed to provide evidence for transmembrane Ca2+ flux or alteration in intracellular levels of cAMP, respectively, as mechanisms for the observed inhibition of hepatocyte taurocholate uptake by VIP. These data, coupled with both clinical and other basic observations, suggest that VIP may play a significant role in the regulation of hepatic bile secretion.

Animals↗
PubMed2004

Dietary plasma protein affects the immune response of weaned rats challenged with S. aureus Superantigen B.

The aim of this study was to determine the potential modulatory effects of diets supplemented with spray-dried animal plasma (SDAP) or immunoglobulin concentrates (IC) on the immune response of rats challenged with Staphylococcus aureus enterotoxin B (SEB). Lewis rats were fed diets containing 80 g of SDAP/kg diet, 22.7 g of IC/kg diet, or milk proteins (Control diet) from postnatal d 21 (weaning) for 14 d. On d 30 and 33, rats were given SEB (0.5 mg/kg body weight; i.p.). Organized gut-associated lymphoid tissue (GALT) populations, intestinal secretion, mucosal and serum immunoglobulin concentrations, and neutrophil infiltration were studied. On d 35, blood was collected under anesthesia and samples of intestinal mucosa, Peyer's patches, mesenteric lymph nodes (MLN), and spleen were taken. SEB increased the water content of feces, which was prevented by diets containing either SDAP (P < 0.002) or IC (P < 0.001), indicating that plasma protein-supplemented diets can reverse the SEB-induced secretory response. In Peyer's patches, the diet containing SDAP partially prevented the SEB-induced increase in T lymphocytes (P < 0.1) and reduced the percentage of activated T helper cells (P < 0.05). In MLN, activated T lymphocytes were increased by SEB but they were not affected by diet. No effects of SEB or dietary supplementation on mucosal IgA and serum IgA and IgG were observed. The effects of SDAP supplementation on the lymphocyte populations of GALT in rats challenged with SEB support the view that SDAP can modulate the immune response and suggest that plasma protein supplementation can prevent GALT from possible activation by luminal bacterial superantigens.

Animals↗
PubMed1998

Differences in immune responses induced by oral and rectal immunizations with Salmonella typhi Ty21a: evidence for compartmentalization within the common mucosal immune system in humans.

Based on the concept of the common mucosal immune system, immunization at various inductive sites can induce an immune response at other, remote mucosal surfaces. The immune responses elicited through rectal and oral routes of antigen delivery were compared with respect to (i) measurement of antibody responses in serum and various external secretions of the vaccinees and (ii) characterization of the nature and homing potentials of circulating antibody-secreting cells (ASC). Specific ASC appeared in the circulation in 4 of 5 volunteers after oral and 9 of 11 volunteers after rectal immunization with Salmonella typhi Ty21a. The kinetics, magnitude, and immunoglobulin isotype distribution of the ASC responses were similar in the two groups. In both groups, almost all ASC (99 or 95% after oral or rectal immunization, respectively) expressed alpha4 beta7, the gut homing receptor (HR), whereas L-selectin, the peripheral lymph node HR, was expressed only on 22 or 38% of ASC, respectively. Oral immunization elicited a more pronounced immune response in saliva and vaginal secretion, while rectal immunization was more potent in inducing a response in nasal secretion, rectum, and tears. No major differences were found in the abilities of the two immunization routes to induce a response in serum or intestinal secretion. Thus, the rectal antigen delivery should be considered as an alternative to the oral immunization route. The different immune response profiles found in various secretions after oral versus rectal antigen administration provide evidence for a compartmentalization within the common mucosal immune system in humans.

Administration, Oral↗
PubMed1995

Synthesis and parallel secretion of rat intestinal alkaline phosphatase and a surfactant-like particle protein.

Rat intestinal microvillous alkaline phosphatases are secreted bidirectionally from the enterocyte attached to a phospholipid-rich membrane (surfactant-like particle). To determine the intracellular pathways for newly synthesized alkaline phosphatases and for the extracellular enzyme-particle complex in the intestinal mucosa, pulse-chase experiments were performed. Synthesis of both isoforms of alkaline phosphatase in fasted rats peaked in the Golgi at 15-30 min and in the microvillous membrane at 60 min, without intermediate localization in the basolateral membranes. A second peak of incorporation was found at 15-30 min in scrapings obtained from the apical surface of the enterocytes. These results demonstrate a dominant direct Golgi-to-microvillous membrane transport for newly synthesized alkaline phosphatase. An additional precursor pool(s) appears responsible for the early appearance of enzyme in the lumen. Newly synthesized alkaline phosphatase isoforms and the 97-kDa protein of surfactant-like particles showed parallel patterns of appearance in enterocytes, luminal washings, and lamina propria after triacylglycerol feeding and were preferentially secreted into the lumen and lamina propria at times (5-7 h) when enterocyte content of these newly synthesized proteins had declined toward basal rates. Enhanced secretion of newly synthesized proteins for hours after fat feeding could explain the prolonged rise in serum and luminal washings of both the enzyme and the particle.

Alkaline Phosphatase↗
PubMed1997

Antisecretory mechanisms of peptide YY in rat distal colon.

Peptide YY (PYY) is a potent regulator of intestinal secretion. These studies investigated the role of Y1 and Y2 receptor subtypes in mediating the antisecretory effects of PYY on mucosa-submucosa preparations of rat distal colon. Addition of vasoactive intestinal peptide (VIP) to these tissues resulted in a 140 +/- 18% increase in basal short-circuit current (Isc) and the induction of Cl- secretion. VIP-stimulated increases in Isc were abolished by the addition of each of PYY, (Pro34)-PYY, a Y1 receptor-selective agonist, and PYY-(3-36), an endogenous Y2 receptor-selective ligand. However, when tissue neural transmission was blocked with tetrodotoxin, neither PYY nor its receptor subtype-selective analogs were able to inhibit VIP-stimulated increases in Isc. These results suggest that in the rat distal colon, the antisecretory actions of PYY are mediated through a combination of Y1 and Y2 receptor subtypes or through a novel receptor subtype that is unable to discriminate between (Pro34)-PYY and PYY-(3-36).

Animals↗
PubMed1978

Diet and cell growth modulation by ammonia.

Fiber is not digested by endogenous enzymes but is fermented by microbes principally in the large intestine. With fermentable energy available, microbes synthesize protein by using ammonia released by their enzymes from urea and other nitrogenous substances in ingesta and intestinal secretions. Fibber fermentation also yields fatty acids that lower the concentration of free ammonia by lowering pH. Fiber increases bulk and water of intestinal contents, shortens transit time, and decreases the concentration of toxic substances in contact with the intestinal mucosa. These processes decrease duration and intensity of exposure of the intestinal mucosa to free ammonia, the form of nitrogen that is most toxic and most readily absorbed by cells. At concentrations found in the lower bowel on usual Western diets, ammonia destroys cells, alters nucleic acid synthesis, increases intestinal mucosal cell mass, increases virus infections, favors growth of cancerous cells over noncancerous cells in tissue culture, and increases virus infections. Ammonia in the bowel increases as protein intake increases. The attributes of ammonia and the epidemiological evidence comparing populations that maintain low intakes of unrefined carbohydrate with those that consume high intakes of protein, fat, and refined carbohydrates implicate ammonia in carcinogenesis and other disease processes.

Ammonia↗
PubMed1992

Epithelial secretory response to inflammation.

As suggested by this and previous reviews, the neuroimmunoregulation of intestinal secretion is a complex series of endocrine, neurocrine, paracrine and autocrine interactions between the underlying cells in the mucosa and submucosa and the intestinal enterocyte. Under normal conditions, the balance of each of these systems is delicately controlled, thus allowing for normal, consistent intestinal function. However, when this finely-tuned system is altered, such as in a diseased state, the resultant effect is an amplification of the host defense response. Initially thought to be protective against further insult, this local immune response, if allowed to continue uncontrollably, can exacerbate the disease process.

Animals↗
PubMed2006

Unconjugated bilirubin modulates the intestinal epithelial barrier function in a human-derived in vitro model.

Unconjugated bilirubin promotes intestinal secretion without affecting nutrient digestion or absorption. In the current study, the effects of unconjugated bilirubin (UCB) on the barrier function of the intestinal epithelium were investigated. The apical side of human intestinal cell line Caco-2 monolayers was challenged with purified UCB. Transepithelial electrical resistance and paracellular fluxes of 10 kD Cascade blue conjugate dextran were measured. Cell monolayer viability was studied using LDH release and trypan blue exclusion tests. Redistribution of enterocyte tight junction occludin was studied by confocal microscopy. Bilirubin induced a dose-dependent decrease of transepithelial electrical resistance (TEER). This effect was maximal at 6 h and tended to be reversed at 48 h. Oxidated bilirubin was ineffective. Bilirubin significantly increased fluorescent dextran paracellular passage. Cell viability was not affected by UCB over the 5-200 nmol/L concentration range. Finally, bilirubin triggered a reversible redistribution of tight junctional occludin. UCB increases the permeability of intestinal epithelium. This effect is reversible, dependent on the redox status of the molecule and the rearrangement of the tight junction. These data attribute to bilirubin a novel role of functional modulator of intestinal paracellular permeability in vitro.

Bilirubin↗
PubMed1982

Preferential transport of IgA and IgA-immune complexes to bile compared with other external secretions.

When radiolabeled dinitrophenyl-human serum albumin was injected intravenously in mice together with M315 IgA, labeled antigen was specifically transported into bile, but not into saliva, urine, milk or bronchial and intestinal secretions. Ultracentrifugal analysis showed that the antigen transported into bile was intact and partly complexed with IgA. The radioactivity that was present in other secretions regardless of M315 IgA, represented free and degraded fragments of antigen. M315 IgA alone was readily transported into bile, where it was detected at high titer by hemagglutination, but not into other secretions, apart from milk which contained only very low titers. The liver therefore appears to be singularly capable of transporting both free and complexed IgA into its secretion, the bile.

Animals↗
PubMed1988

Effect of cigarette smoking on extent of acid-secreting area and intestinal metaplasia in the stomach.

The association of cigarette smoking and other variables with the extent of the acid-secreting area and intestinal metaplasia were investigated by multivariate analysis. Studies were made by the endoscopic Congo red-methylene blue test developed in our hospital. In this test, acid-secreting areas and areas of intestinal metaplasia could be identified as discolored areas and areas staining blue with methylene blue, respectively. In multivariate analysis, the following variables were associated with a reduction in the size of the acid-secreting area in decreasing order of importance: the smoking index and age. The following factors had little or no influence on the size of the acid-secreting area: sex, and the consumption of aspirin and nonsteroidal, nonsalicylate, antiinflammatory drugs (NSNSAIDs). In general, in patients with a high smoking index, the acid-secreting area was small. Smoking had an influence in both younger and older patients and had more influence in females than in males. Multivariate analysis also shows that the following factors were associated with an increase in the area of intestinal metaplasia in decreasing order of importance: the extent of the acid-secreting area, age, and the smoking index. The following factors had little or no influence on the area of intestinal metaplasia: the consumption of aspirin and NSNSAIDs and sex. In general, in patients with little or no acid-secreting area, the area of intestinal metaplasia was extensive. These findings indicate that smoking is associated with reduction in the size of the acid-secreting area and so in development of intestinal metaplasia.

Adult↗
PubMedDate not supplied

Intestinal immunomodulation by vitamin A deficiency and lactobacillus-based probiotic in Eimeria acervulina-infected broiler chickens.

In a 2 X 2 factorial study, a broiler starter ration was amended for vitamin A (control, C; deficient, A) and probiotic status (-, P) to investigate their modulatory effects onthe host immune system. Birds were inoculated orally with Eimeria acervulina (EA) oocysts, and disease susceptibility was evaluated by assessment of fecal oocyst shedding. Humoral and local cellular mediated immunity were assessed by evaluation of antibody and cytokine (interferon-gamma [IFN-gamma] and interleukin-2 [IL-2]) levels in sera and intestinal secretions on a 3-day interval after inoculation. Fecal oocyst shedding was highest (P < 0.05) in A- birds, followed by AP, C-, and CP birds. Feeding the probiotic reduced shed oocysts by 20% in A fed birds and by 26% in C fed birds. Intestinal IFN-gamma was relatively constant in all treatment groups except for A-, where it declined steadily and was lower (P < 0.05) from day 6 on. Serum IFN-gamma levels fluctuated within each treatment and over time were not revealing. Intestinal IL-2 was highest in CP birds at 3 and 9 days postinfection (DPI) and lowest in A- birds at 3, 9, and 12 DPI (P < 0.05); no difference between treatments was found at 6 DPI (P > 0.05). Eimeria-specific intestinal antibody (Ab) level was constant (P > 0.05) in C- birds but increased with time (P < 0.05) in A-, AP, and CP birds. Serum Ab levels were also constant in A- and CP birds but increased (P < 0.05) in C- and AP birds after 6 DPI. The data demonstrate for the first time a probiotic-enhanced immunity in vitamin A deficient birds. This study is also the first to demonstrate the probiotic effect on local cell-mediated immunity of chickens, best manifested by apparent lower intestinal invasion and development by EA, on the basis of higher IL-2 secretion and lower EA oocyst production.

Animals↗