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At least 1,063 records · Page 59Linked to original sources
PubMed2006

Chronic psychological stress in rats induces intestinal sensitization to luminal antigens.

There is increasing evidence that stress plays a role in the pathophysiology of chronic intestinal disorders, but the mechanisms remain unclear. Previous studies in rats have revealed that stress decreases gut barrier function and allows excessive uptake of luminal material. Here, we investigated whether chronic psychological stress acts to induce sensitization of intestinal tissues to oral antigens. Rats were subjected to 1 hour per day of water avoidance stress or sham stress daily for 10 days, and horseradish peroxidase (HRP) was delivered by gavage on day 5. Studies to determine sensitization were conducted on day 20. All stressed rats developed HRP-specific IgE antibodies, antigen-induced intestinal secretion, and increased numbers of inflammatory cells in gut mucosa. Luminal HRP was absorbed more readily by enterocytes of stressed animals. In addition, stressed rats had increased expression of interleukin-4 and decreased expression of interferon-gamma in gut mucosa, a cytokine profile that is typical of allergic conditions. Treatment of stressed rats with an antagonist to corticotropin-releasing hormone (previously shown to inhibit stress-enhanced gut permeability) eliminated the manifestations of intestinal hypersensitivity. Our results indicate that the presence of oral antigen during chronic psychological stress alters the immune response (to sensitization rather than oral tolerance) and causes subsequent antigen-induced gut pathophysiology.

Animals↗
PubMed1984

Administration of purified colonization factor antigens (CFA/I, CFA/II) of enterotoxigenic Escherichia coli to volunteers. Response to challenge with virulent enterotoxigenic Escherichia coli.

Colonization factor antigens (CFAs) were administered orally to volunteers, and the mucosal immune response was assessed by measuring secretory immunoglobulin A (IgA) in saliva and intestinal secretions and by challenge with virulent enterotoxigenic Escherichia coli (ETEC). A combination of CFA/I and CFA/II (8 mg each) administered orally in four doses in milk failed to induce a mucosal IgA response and also failed to protect against challenge with CFA-positive ETEC. When CFA was administered orally (1.5 mg divided into three doses with bicarbonate) to volunteers without preexisting serum anti-CFA levels, it failed to elicit a serum IgG or intestinal secretory IgA response or to protect against challenge with virulent ETEC. The CFA is destroyed by acid gastric contents but it induced significant antibody titer rises in 8 of 11 (73%) volunteers with preexisting serum anti-CFA IgG levels after oral administration of 1 mg of CFA/I with sodium bicarbonate. Subcutaneous priming (50 micrograms CFA/I) did not induce a serum IgG response but, when followed by oral boosting (1 mg CFA/I in two divided doses with sodium bicarbonate), induced intestinal anti-CFA secretory IgA in 4 of 8 volunteers and protected against challenge with CFA/I-positive ETEC. These results, although preliminary, are encouraging and demonstrate that it may be possible to develop an effective oral vaccine based on soluble nonreplicating antigens such as purified CFAs.

Administration, Oral↗
PubMed2005

Expression of human TFF3 in relation to growth of HT-29 cell subpopulations: involvement of PI3-K but not STAT6.

The trefoil factor family (TFF) peptides 1 and 2 (TFF1 and 2) are expressed in mucus cells of the stomach, whereas TFF3 is localized in goblet cells of the intestine. In the present study, we aimed to determine whether phosphatidylinositol 3-kinase (PI3-K) or signal transducer and activator of transcription protein 6 (STAT6) is involved in the expression of goblet cell specific markers. TFF3 expression was analyzed by RT-PCR, Northern blot, and radioimmunoassay (RIA) in relation to cell growth in subclones of HT-29 cells including the CL.16E and methotrexate (MTX) cell lines, which both exhibit a phenotype of mucus-secreting intestinal cells. A 30-fold increase in TFF3 mRNA levels and a 10-fold increase in TFF3-cell content were observed between the early proliferative and the late confluency states. The levels of MUC2 and MUC3 mRNA were also increased in the course of the differentiation process. A three to fourfold increase in PI3-K and Akt activities was observed in early post-confluent cells as compared with pre-confluent cells. Exposure of pre- and post-confluent cells to LY294002, a specific PI3-K inhibitor, for 1-4 days profoundly reduced TFF3 and MUC2 expression. A marked reduction in mucin granules content was also observed in LY-treated cells. Inhibition of the mitogen-activated protein (MAP) kinase kinase (MEK) with PD98059 did not modify the course of differentiation of the goblet cell lines. Moreover, stable transfection of HT-29 CL.16E cells with a dominant negative form of STAT6 had no effect on TFF3 induction. Together, these data indicate that PI3-K promotes the expression of TFF3 and MUC2 and that the PI3-K/Akt pathway may play a pivotal role in intestinal goblet cell differentiation.

Cell Differentiation↗
PubMed1986

Malabsorption of long-chain fatty acid in cholera toxin-induced secretory diarrhea.

The effects of cholera toxin-induced diarrhea on the absorption of fatty acids of different chain lengths were investigated using rat small intestine. In the study using isolated jejunal loops, the absorption of the long-chain fatty acid, linoleic acid, into the intestinal mucosa was significantly impaired 90 min after the administration of linoleic acid micelles in the cholera toxin-treated rats. This reduction of linoleic acid absorption in the cholera toxin-treated rats was not found at 180 min. We could not find any mucosal accumulation of labeled linoleic acid or disturbance of triglyceride formation in the intestinal mucosa as compared with that of controls. The amount of linoleic acid transported into the intestinal lymph was delayed and reduced in cholera toxin-treated rats. Furthermore, the absorption of the medium-chain-length fatty acid, octanoic acid, was unchanged in the cholera toxin-treated rats. These results suggest that intestinal secretion induced by cholera toxin may delay the mucosal uptake and lymphatic transport of long-chain fatty acids. Cholera toxin may not affect triglyceride formation in the epithelial cells.

Animals↗
PubMed2001

Enhanced systemic and mucosal antibody responses to a model protein antigen after intranasal and intratracheal immunisation using Bacillus firmus as an adjuvant.

Bacillus firmus, a non-pathogenic Gram positive (G+) bacterium of the external environment was investigated for immunomodulatory properties. It stimulated an increase in anti-ovalbumin IgG in sera, bronchoalveolar lavages and intestinal washings after both intranasal (i.n.) and intratracheal (i.t.) immunisation, and enhanced anti-ovalbumin IgA in intestinal secretions and in bronchoalveolar lavage fluid after i.n. or i.t. immunisation, respectively. The immunomodulatory effect of B. firmus on antibody formation was antigen specific.

Adjuvants, Immunologic↗
PubMed2003

Secretin, 100 years later.

One hundred years have elapsed since the discovery of secretin by Bayliss and Starling in 1902. In the past century, the research of secretin has gone by many milestones including isolation, purification and structural determination, chemical synthesis, establishment of its hormonal status by radioimmunoassay and immunoneutralization, identification of the specific receptor, cloning of secretin and its receptor, and identification of a secretin-releasing peptide. It has become clear that secretin is a hormone-regulating pancreatic exocrine secretion of fluid and bicarbonate, gastric acid secretion, and gastric motility. The release and actions of secretin is regulated by hormone-hormonal and neurohormonal interactions. The vagus nerve, particularly its afferent pathway, plays an essential role in the physiological actions of secretin. Substantial information about the property of the secretin receptor has been accumulated, but a potent secretin receptor-specific antagonist remains to be formulated. The neural regulatory mechanisms of the release and action of secretin await further elucidation. The physiological role of secretin in intestinal secretions and motility and extragastrointestinal organs remains to be defined. The presence of secretin and its receptor in the central nervous system is well documented, but its function as a neuropeptide has been recognized gradually and requires extensive study in the future.

Animals↗
PubMed1992

Salivary IgA antigliadin antibody as a marker for coeliac disease.

In recent years, serum antibodies to gliadin (AGA) have been reported to be useful markers of coeliac disease. IgA AGA have also been found in intestinal secretions and saliva in coeliac disease and may offer a convenient, non-invasive screening test. In order to test this hypothesis, salivary and serum AGA were measured in children with coeliac disease proved by biopsy and compared with several control groups. Measurement of salivary IgA AGA provided excellent discrimination between those children with coeliac disease and the control groups, and our study suggests that it may provide a rapid, non-invasive method of screening for this disease before intestinal biopsy.

Adolescent↗
PubMed1990

Octreotide inhibits increases in short-circuit current induced in rat colon by VIP, substance P, serotonin and aminophylline.

We investigated the effect of octreotide (OCT), a stable somatostatin analog, (OCT) on changes in short-circuit current (Isc) induced by vasoactive intestinal peptide (VIP), aminophylline, serotonin (5-HT) and substance P. OCT significantly decreased basal Isc at a concentration of 10(-9) M; the maximum decrease in Isc was observed at 10(-6) M. OCT (10(-7) M) significantly inhibited the intestinal secretory response to all the secretagogues studied. The maximum Isc response was reduced when tissues were stimulated with VIP (184.9 +/- 18.0 vs. 119.7 +/- 14.1, P less than 0.05), 5-HT (135.1 +/- 14.4 vs. 79.5 +/- 13.4, P less than 0.05) and substance P (156.0 +/- 19.2 vs. 30.7 +/- 5.4, P less than 0.01). In the case of aminophylline, the concentration-response curve was shifted to the right but the maximum response was not reduced. Because VIP and aminophylline increase cAMP while 5-HT and substance P stimulate intestinal secretion principally by a calcium linked mechanism, we conclude that OCT inhibits Isc in rat colon by more than one mechanism.

Aminophylline↗
PubMed1977

Failure of glucagon to influence ion transport across human jejunal and ileal mucosa in vitro.

Glucagon (90 to 880 pg.ml-1) failed to influence electrical activity or fluxes of sodium and chloride across human jejunal and ileal mucosa in vitro. These results suggest that the intestinal secretion and diarrhoea produced in vivo in man during intravenous infusion of glucagon may be produced by changes in motility and blood flow and not directly by activating an ion secretory mechanism as is the case in cholera.

Biological Transport, Active↗
PubMed1998

Role of small intestine in caloric compensations to oil premeals in rats.

We postulated that dose-responsive satiety after oil premeals varies with the number of gut sensors stimulated by lipolytic products along intestine. These experiments in fasted rats on satiety after oil premeals were performed to 1) determine whether satiety was induced by lipolytic products but not triglycerides; 2) confirm that oil empties from the stomach at rates that vary with oil loads; 3) ascertain that increasing rates of oil entry into duodenum extend the length of gut contacted by lipolytic products; and 4) judge whether length of gut contacted correlated with dose-responsive satieties to dietary oils. 5) Using specific antagonists, we attempted to define how satiety was signalled by gut sensors. Timing and degrees of satiety did not correlate with timing and extent of gastric distensions but, rather, with the timing and extent of spread of lipolytic products along small bowel. Satiety after the highest premeal load of oil was blocked by Pluronic L-81, an inhibitor of intestinal secretion of apolipoprotein A-IV, but was unaffected by MK-329 (a specific antagonist of cholecystokinin) or by capsaicin blockade of chemosensory nerves.

Analysis of Variance↗
PubMed1998

The specificity of antibody in chickens immunised to reduce intestinal colonisation with Campylobacter jejuni.

Poultry consumption has been identified as a major risk factor for human infection with Campylobacter jejuni in developed countries. C. jejuni is present in the gastrointestinal tract of broiler chickens at the time of slaughter, and faecal contamination of carcases during processing results in significant campylobacter loads on carcases. One approach to reducing the level of carcase contamination with C. jejuni is to control campylobacter infection in broiler chickens. To this end, the study described here investigated the specificity of antibody in serum and intestinal secretions of chickens that had been immunised with campylobacter antigens and then challenged with viable bacteria. The immunodominant antigens in the serum of birds that showed a 2-log reduction in caecal colonisation with C. jejuni included flagellin protein (61-63 Kd) and three additional antigens of 67, 73.5 and 77.5 Kd. Only flagellin and the 67 Kd antigen were recognised by IgG antibody in gastrointestinal secretions of the same birds. Antibody from chickens immunised with purified native flagellin protein recognised flagellin protein and the 67 Kd antigen in Western blots probed with serum, but only the flagellin proteins (61-63 Kd) in Westerns probed with gastrointestinal secretions. Analysis of the specificity of the response to flagellin protein using recombinant clones that expressed regions of the flagellin gene suggests that epitopes in each region of the flagellin protein were immunogenic. Of the immunodominant antigens, only flagellin appeared to be surface-exposed on viable C. jejuni, although conformational epitopes of flagellin appeared to be sensitive to the method of antigen purification. The results of this study suggest that flagellin and possibly the 67 Kd antigen may be valuable for immunological control of intestinal infection with C. jejuni in chickens, but that further work is required to purify these as vaccine candidates by using methods that preserve conformational epitopes.

Animals↗
PubMed1992

Fibroblasts modulate intestinal secretory responses to inflammatory mediators.

Cultured colonic epithelial cells and fibroblasts were used to examine the interaction between these cell types during intestinal secretion. Secretory responses of T84 colonic epithelial cells, measured as changes in the short-circuit current in modified Ussing chambers to bradykinin, serotonin, hydrogen peroxide, and histamine, were enhanced in the presence of fibroblasts, either in cocultures or when separate cultures of fibroblasts were acutely juxtaposed with the T84 cultures. This effect was abolished by pretreatment with indomethacin and the fibroblasts were found to release prostaglandin E2 in response to these inflammatory mediators. Fibroblasts may exert a paracrine regulation on the secretory response of intestinal epithelial cells via the generation and release of cyclooxygenase products in response to inflammatory mediators. These studies suggest a novel function for the intestinal fibroblastic sheath: that of amplification of the inflammatory response through mesenchymal/epithelial interaction.

Animals↗
PubMed1997

Effects of insulin-like growth factor I (IGF-I) on the small intestine: a comparison between oral and subcutaneous administration in the weaned rat.

Several studies have suggested that growth factors play an important role in the development and the maintenance of the gastrointestinal tract. Colostrum and normal breast milk as well as intestinal secretion are reported to contain IGF-I. Thus, the objective of this study was to investigate whether the route of administration of IGF-I, subcutaneously and orally, was important for the way of influencing the gastrointestinal tract in the weaned rat and further to observe if this effect was affected by different feed regimens. Well nourished weaned rats subcutaneously administered IGF-I (2 mg/kg body weight and day during 14 days) were found to have significantly increased relative weights of the small intestine, increased duodenal crypt depths and villi heights compared with control rats. The same dose given orally in bovine milk had no effect. Furthermore, a study was performed with the same dose of IGF-I given for 7 days together with a restricted feed regimen. Similar observations, although of a slightly smaller magnitude, were found. These observations indicate that the effect of IGF-I on gastrointestinal renewal in the weaned rat is not depending on an IGF-I supply through the gastrointestinal fluids but rather through a supply via the circulation or by a local intestinal production. The effects were statistically significant both in well fed and malnourished conditions.

Administration, Oral↗
PubMed2004

Loperamide modifies the tissue disposition kinetics of ivermectin in rats.

Ivermectin (IVM) is a broad-spectrum antiparasitic drug extensively used in human and veterinary medicine that is largely excreted in bile and faeces. Loperamide (LPM) is an opioid derivative that reduces gastrointestinal secretions and motility. Both IVM and LPM have been reported to act as P-glycoprotein substrates (P-GP). The goal of the present work was to study the LPM-induced modifications to the pattern of tissue distribution for IVM. Thirty-six Wistar male rats were randomly allocated to two groups (n = 18) and treated subcutaneously with IVM alone or co-administered with LPM. Rats were killed at different times post-treatment and samples (blood and tissues) were collected and analyzed by HPLC. The presence of LPM induced a marked enhancement in the IVM plasma concentrations, resulting in a significantly higher area under concentration time curve (AUC) value (P < 0.01) than that obtained after the administration of IVM alone. Significantly higher IVM availabilities in the liver tissue and small intestine wall (P < 0.05) were obtained in the presence of LPM. There were no statistically significant differences in drug availability in the large intestinal wall after both treatments. However, LPM induced a marked decrease in the amount of IVM recovered in the large intestinal lumen content. The ratio between IVM concentrations in the large intestinal luminal content and plasma at day 1 post-treatment was 4.64-fold higher in the absence of LPM. The delayed intestinal transit time caused by LPM accounting for an extended plasma-intestine recycling time, and a potential competition between IVM and LPM for the P-GP-mediated bile-intestinal secretion processes, may account for the enhanced IVM systemic availability reported in the current study.

Animals↗
PubMed1977

Effect of enteric micro-organisms on intestinal sugar and fatty acid absorption.

The effect of micro-organisms contaminating the upper intestinal contents of malnourished children on intestinal absorption of 3-0 methyl-alpha-D-glucopyranose (3-M.G.) and oleic acid was studied in rats in vivo. Oleci acid absorption was unaffected by non-pathogenic E. coli but decreased by E. coli 0111, Salmonella paratyphi B., Shigella sonnei and Candida sp. This effect was probably explained by intestinal secretion diluting the test solution leading to a decreased diffusion gradient for solubilised fatty acid. Inhibition of sugar absorption occurred with bacterial suspensions of Staphylococcus aureus, Streptococcus faecalis, E. coli and Candida sp. and cell-free preparations of Staphylococcus aureus, Streptococcus faecalis, a non-pathogenic E. coli, Proteus sp., Klebsiella sp., Pseudomonas sp. and Candida sp. These effects were not explained by dilution of the test solution. This indicates that numerous micro-organisms and, in some instances, their cell-free preparations can interfere with intestinal active sugar transport. These findings may be relevant to the production of malabsorption in malnourished children who have a wide variety of micro-organisms contaminating their upper intestinal contents.

Animals↗
PubMed1984

[Effect of guar flour on endogenous nitrogen excretion in rats determined by the 15N-tracer technic].

The metabolic fecal nitrogen was determined in 8 young rats (90-100 g body weight) using a single oral dose of 75 mg 15N-glycine. Four rats were fed a diet containing 8% guar and 4 rats received a control diet without guar. Compared to the control group, apparent protein digestibility and nitrogen balance were significantly lower in the guar group. After an initial steep rise the 15N-elimination in feces and urine (days 2-8 after 15N-glycine application) followed an exponential curve in at least 2 phases, with increasing half-time values. The proportion of metabolic fecal nitrogen to total fecal nitrogen was calculated from the 15N-atom-% excess, determined daily in urine and in feces. This calculation is based on the assumption that the specific 15N-activity (15N-atom-% excess) in urine represents the specific 15N-activity of the endogenous nitrogen pool. The addition of guar raised the proportion of metabolic fecal nitrogen from 51% (control) to 73%, corresponding to an increase in total fecal nitrogen loss (24 mg) observed in the guar-fed animals. This indicates that the rise in fecal nitrogen loss caused by guar is due almost entirely to enhanced secretion of endogenous nitrogen and not to undigested food protein. Based on the analysis of 2,6-diamino-pimelic acid in the feces of 4 rats the proportion of bacterial nitrogen in the feces was calculated. It amounted to 19.8% of total fecal N in the control group, and to 30.1% in the guar group, or to 39.4% and 44.4% of metabolic fecal nitrogen respectively. Obviously the increased dietary fiber intake also caused a rise in the amount of metabolic fecal nitrogen, which is derived from gastro-intestinal secretions and epithelial tissue.

Animals↗
PubMed2004

Targeting nitric oxide in the gastrointestinal tract.

This review discusses the contributions of the three nitric oxide (NO) synthase (NOS) isozymes neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS) to the function and diseases of the gastrointestinal tract. Small (nanomolar) quantities of NO produced by calcium-dependent nNOS play a physiological role in peristalsis and sphincter function of the intestine. Decreased nNOS function can result in aperistalsis and obstructive sphincters. NO produced by eNOS dilates mucosal blood vessels and prevents leukocyte aggregation, and is therefore essential for the maintenance of mucosal blood flow. Absence of eNOS-derived NO results in an increased susceptibility of the gastrointestinal tract to injury. Selective NO delivery by gene therapy or NO-donating compounds may offer new therapeutic options in motility disorders of the gut and the prevention of mucosal injury. The effects of large (micromolar) amounts of NO as produced by iNOS are less well understood. Large amounts of NO can increase gut permeability, induce apoptosis and stimulate intestinal secretion, while NO can also kill bacteria, block apoptosis and reduce inflammation by inhibiting activation of nuclear factor-kappaB (NFkappaB). Lumenal donation of NO could therefore block NFkappaB activation and be a treatment option in inflammatory conditions of the bowel.

Animals↗
PubMed2004

Characterization of jejunal absorption and apical efflux of ropivacaine, lidocaine and bupivacaine in the rat using in situ and in vitro absorption models.

The purpose of this study was to characterize the rat jejunal passive transport and the possible active efflux of three local anaesthetics, ropivacaine, lidocaine and bupivacaine using two different absorption models, the in situ single-pass intestinal perfusion and the in vitro Ussing chamber model, as well as P-glycoprotein (Pgp)-mediated calcein transport inhibition in Caco-2 cells. Concentration and pH dependence, efflux inhibition by verapamil and digoxin and bi-directional permeability studies were performed to investigate the potential involvement of efflux carriers in the intestinal absorption of the local anaesthetics. In the jejunal perfusion the permeability of these agents appeared to be high, predicting complete intestinal absorption (>90%). There was no effect of the Pgp inhibitors on net absorption for any of the local anaesthetics in the two absorption models. However, in the Ussing chamber at an equal pH of 7.4 at mucosal and serosal sides, the observed jejunal permeability ratios (S-M)/(M-S), of 2.3, 1.8 and 3.0 for ropivacaine, lidocaine and bupivacaine, respectively, indicated at least some involvement of carrier-mediated intestinal secretion. This idea was supported in the calcein AM Pgp transport assay in which two of the tested local anaesthetic agents affected cellular calcein retention. As anticipated for these agents, the mucosal pH conditions were shown to largely affect the gut permeability. The jejunal permeabilities of the local anaesthetics as measured in the two absorption models fitted well in a model comparison that incorporated the permeabilities of six other structurally unrelated drugs. In conclusion, the jejunal permeability of ropivacaine, lidocaine and bupivacaine was high and although evidence was obtained for carrier-mediated intestinal efflux this process appeared not to have a significant influence on the rate and extent of in vivo intestinal absorption. Rather, passive diffusion of these agents seems to be the major mechanism for the intestinal absorption.

Amides↗