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PubMed1987

Intestinal mucosal mast cells in normal and nematode-infected rat intestines are in intimate contact with peptidergic nerves.

Inflammatory or allergic conditions, as well as situations where healing and repair processes occur, are characterized by the presence of increased numbers of mast cells. Previous work on the effect of neuropeptides on mast cell mediator release showed that only substance P caused such release from intestinal mucosal mast cells [Shanahan, F., Denburg, J. A., Fox, J., Bienenstock, J. & Befus, A. D. (1985) J. Immunol. 135, 1331-1337]. Accordingly, we investigated the microanatomical relationship between mast cells and enteric nerves in normal rat intestine and parasite-infected rat intestine, in which mucosal mast cell hyperplasia occurs. Combined immunohistochemistry for neuron-specific enolase and staining with alcian blue at pH 0.5 was employed on paraffin-embedded sections of normal and Nippostrongylus brasiliensis-infected rat jejunum. Sixty-seven percent of intestinal mucosal mast cells were touching subepithelial nerves, and an additional 20% were within 2 micron of nerves. Assessment of the proportion of the lamina propria occupied by mast cells (12.5%), the average mast cell area (121 +/- 28 microns 2), and the density of enteric nerves (one per 788 +/- 151 microns 2) suggested that the association was 5 times greater than would be expected by chance alone (P less than 0.0001). In consecutive sections, the nerves in contact with mast cells were also shown to contain substance P and/or calcitonin-gene-related peptide. Electron microscopy confirmed this association: 8% of the mast cells in infected rats exhibited membrane-membrane contact with unmyelinated axons containing 70- to 170-nm dense-core vesicles, and an additional 31% were situated less than 250 nm from nerves. Other mast cells appeared to embrace nerve bundles through the projection of lamellopodia. These data provide systematic quantitative evidence that a structural foundation for communication between the immune and nervous systems exists in the rat gastrointestinal tract.

Animals↗
PubMed1998

Intestinal trefoil factor induces inactivation of extracellular signal-regulated protein kinase in intestinal epithelial cells.

Intestinal trefoil factor (ITF), a small, compact protease-resistant peptide, is abundantly expressed in goblet cells of large and small intestine. Although several biological activities of ITF have been identified, including promotion of wound healing, stimulation of epithelial cell migration, and protection of intestinal epithelial barrier, little is known about signaling events through which ITF mediates its physiological function. In this study, the effects of exogenous ITF on mitogen-activated protein kinase (MAPK) signaling cascades were examined in IEC-6 cells, a nontransformed intestinal epithelial cell line that does not express endogenous trefoil peptides. Stimulation with ITF resulted in rapid decrease in extracellular signal-related protein kinase (ERK) activity and concomitant reduced ERK tyrosine phosphorylation. ITF also decreased activation of ERK activity induced by either transforming growth factor-alpha, which links extracellular stimuli to the Ras/Raf/MEK/ERK pathway via the epidermal growth factor receptor, or phorbol 12-myristate 13-acetate, which activates Raf through protein kinase C. ITF-induced inhibition of ERK activity was blocked by an inhibitor of tyrosine and dual-specific phosphatases, sodium orthovanadate. In summary, ITF leads to inhibition of ERK and the MAPK pathway through activation of tyrosine or dual-specific phosphatase.

Calcium-Calmodulin-Dependent Protein Kinases↗
PubMed2006

Vangl1 protein acts as a downstream effector of intestinal trefoil factor (ITF)/TFF3 signaling and regulates wound healing of intestinal epithelium.

The intestinal trefoil factor (ITF/TFF3) protects intestinal epithelia from a range of insults and contributes to mucosal repair. However, the signaling events that mediate healing responses are only partially understood. To identify ITF signaling pathways, proteins that were Ser/Thr phosphorylated in response to ITF stimulation were immunoprecipitated from human colon carcinoma cell lines and identified by mass spectrometry. We demonstrated that Van Gogh-like protein 1 (also designated Vang-like 1 or Vangl1), a protein with four transmembrane domains, was Ser/Thr phosphorylated in response to ITF stimulation. Vangl1 was present in normal human colon and all intestinal epithelial cell lines (IEC) tested. In transfected IEC, FLAG-Vangl1 was mostly present in the Nonidet P-40 soluble fraction as detected by Western blotting, corresponding to the localization of endogenous protein in cytoplasmic vesicular structures by confocal microscopy with rabbit polyclonal anti-human Vangl1 antibody (alpha-Vangl1). Vangl1 cell membrane association increased with differentiation, as demonstrated by co-localization with E-cadherin in differentiated IEC. Increased Vangl1 phosphorylation after stimulation with ITF corresponded to decreased cell membrane association with E-cadherin. Functionally, Vangl1 overexpression enhanced ITF unstimulated and stimulated wound closure of IEC, whereas siRNA directed against Vangl1 inhibited the migratory response to ITF. Vangl1 protein may serve as an effector mediating the ITF healing response of the intestinal mucosa.

Animals↗
PubMed1990

Effect of hemorrhagic shock on bacterial translocation, intestinal morphology, and intestinal permeability in conventional and antibiotic-decontaminated rats.

Bacterial translocation and ileal and cecal injury have been shown to occur 24 h after limited periods of hemorrhagic shock. The present studies were performed to determine the temporal sequence of mucosal injury, permeability, and bacterial translocation after hemorrhagic shock. The results indicated that bacterial translocation and mucosal injury have occurred by 2 h after a 30-min episode of shock (mean arterial pressure 30 mm Hg). Although the histologic extent of the intestinal mucosal injury was less at 2 h postshock than at 24 h postshock, at both times intestinal barrier function was lost as measured by permeability to horseradish peroxidase. Since the role of translocating bacteria in potentiating the loss of intestinal barrier function after shock is unclear, the second goal was to determine whether the extent of shock-induced mucosal injury and permeability could be reduced or abrogated by antibiotic decontamination of the gut. The extent of shock-induced mucosal injury and intestinal permeability was similar between rats with a normal gut flora (greater than 10(6) bacteria/g cecum) and antibiotic-decontaminated rats (less than 10(3) bacteria/g cecum) 2 h postshock, although the incidences of bacterial translocation were 67% and 0, respectively. Thus, shock-induced mucosal permeability and injury appear not to be directly related to the presence of translocating bacteria.

Animals↗
PubMed2006

Intestinal edema decreases intestinal contractile activity via decreased myosin light chain phosphorylation.

OBJECTIVE: The purpose of this study was to investigate the effects of interstitial edema on intestinal contractile activity. DESIGN: Randomized animal study. SETTING: University laboratory. SUBJECTS: Male Sprague-Dawley rats. INTERVENTION: Intestinal edema was induced in rats by a combination of fluid infusion and mesenteric venous hypertension. Rats were divided into four groups: CONTROL, sham; RESUS, saline infusion only; RESUS+VH, saline infusion and venous hypertension; and VH, venous hypertension only. Edema development, basal contractile activity, maximum agonist-induced contractile response (measured as total force generation during the first 2 mins after carbachol treatment), and myosin light chain phosphorylation were measured in the distal small intestine. MEASUREMENTS AND MAIN RESULTS: The amount of interstitial fluid, indicated by the wet-to-dry ratio, increased significantly in both the RESUS and RESUS+VH groups as early as 30 mins after surgery compared with the CONTROL group. Whereas the tissue fluid remained significantly elevated in the RESUS+VH group up to 6 hrs after surgery, the RESUS group wet-to-dry ratios returned to CONTROL group levels by 2 hrs after surgery. Basal contractile activity was significantly less in the RESUS+VH group compared with either the RESUS group or the CONTROL group 6 hrs after surgery. Maximum contractile response decreased significantly in the RESUS+VH group compared with the RESUS group. Basal contractile activity and maximum contractile response did not change significantly in the VH group compared with the CONTROL group. The phosphorylated fraction of myosin light chain was significantly lower in the RESUS+VH group compared with the CONTROL group at 0.5, 2, and 6 hrs after surgery. CONCLUSION: We conclude that edema decreases myosin light chain phosphorylation, leading to decreased intestinal contractile activity.

Analysis of Variance↗
PubMed2004

The herbal preparation STW 5 (Iberogast) desensitizes intestinal afferents in the rat small intestine.

INTRODUCTION: Visceral hypersensitivity in the upper gastrointestinal tract is a potential pathomechanism of functional dyspepsia. The herbal preparation STW 5 (Iberogast) provides symptomatic relief for this condition. We aimed to investigate whether STW 5 modulates intestinal afferent sensitivity. METHODS: The herbal preparation STW 5 or vehicle (30.8% ethanol) were administered orally in male Wister rats. After 2 h animals were anaesthetized and extracellular multi-unit intestinal afferent nerve recordings were secured from the neurovascular bundle of the mesentery in the proximal jejunum. Afferent discharge to ramp distension of the intestinal loop (0-60 cm H2O) and dose-response curves for i.v. bradykinin (10, 20 and 40 microg kg(-1)) and 5-HT (5, 10, 20 and 40 microg kg(-1)) were recorded. RESULTS: Baseline discharge was not different between the vehicle and treatment group. Ramp distension was followed by a pressure dependent increase in afferent nerve discharge that was decreased following STW 5 pretreatment for all distending pressures reaching 147 +/- 8 impulses s(-1) (imp s(-1)) following STW 5 vs 171 +/- 5 imp s(-1) following vehicle at 60 cm H2O (mean +/- SEM; P < 0.05). A dose-dependent increase in afferent discharge was observed for 5-HT and bradykinin. Following STW 5 pretreatment, afferent discharge was reduced at all doses of 5-HT to 110 +/- 5 at the maximum dose after STW 5 and 128 +/- 3 imp s(-1) in controls (all P < 0.05). Afferent discharge to bradykinin was similarly reduced at 20 and 40 microg kg(-1) but not at 10 microg kg(-1) of bradykinin with a discharge rate of 176 +/- 7 imp s(-1) following STW 5 and 200 +/- 6 imp s(-1) in controls at 40 microg kg(-1) (P < 0.05). CONCLUSIONS: The preparation STW 5 reduces intestinal afferent nerve discharge following chemical and mechanical stimuli, while baseline discharge is not affected. This effect of STW 5 on afferent sensitivity may contribute to its therapeutic relief of dyspeptic symptoms.

Animals↗
PubMed1995

Ca(2+)-independent cytotoxicity of Vibrio parahaemolyticus thermostable direct hemolysin (TDH) on Intestine 407, a cell line derived from human embryonic intestine.

The effects of Vibrio parahaemolyticus thermostable direct hemolysis on Intestine 407, a cell line derived from the intestine of human embryos, were investigated. The hemolysin was shown to be cytotoxic to Intestine 407. This cytotoxicity is accompanied by the damage of plasma membrane and lysosomes, as well as cellular degeneration in the form of large transparent blebs. Although an increase in cytosolic free Ca2+ due t the influx of extracellular Ca2+ was observed in cells treated with thermostable direct hemolysin, it was found to be irrelevant to any of the above effects. These results suggest that the effects of thermostable direct hemolysin observed in this study on Intestine 407 are not mediated by Ca(2+)-dependent pathways.

Bacterial Toxins↗
PubMed1986

Sympathetic nerve activation decreases the release of vasoactive intestinal polypeptide from the feline intestine.

The splanchnic nerves to the small intestine were stimulated in anaesthetized cats. Activation of the sympathetic nerves caused vasoconstriction, increased net fluid absorption and decreased release of vasoactive intestinal polypeptide (VIP) in the small intestine. In the colon, parasympathetic nerve stimulation elicited vasodilatation and increased release of VIP. Additional stimulation of the sympathetic lumbar colonic nerves decreased the colonic blood flow and inhibited the release of VIP. These effects of the stimulation of the lumbar colonic nerves were blocked by phentolamine. It is concluded that, in the feline intestine, sympathetic nerve stimulation presynaptically decreased the release of VIP via an alpha-adrenergic mechanism.

Adrenergic alpha-Antagonists↗
PubMed2000

Stimulation by portal insulin of intestinal glucose absorption via hepatoenteral nerves and prostaglandin E2 in the isolated, jointly perfused small intestine and liver of the rat.

Insulin infused into the portal vein acutely enhanced intestinal glucose and galactose absorption via the sodium-dependent glucose cotransporter-1 in the isolated, jointly perfused small intestine and liver of the rat. Atropine and tetrodotoxin infused into the superior mesenteric artery completely prevented the portal insulin-dependent increase in intestinal glucose absorption, and carbachol caused an increase similar to that of portal insulin. Thus, a signal was transmitted against the bloodstream in a retrograde direction from the portal vein to the small intestine via hepatoenteral cholinergic nerves. The intracellular messenger in the enterocytes was cAMP, and the link between the muscarinic receptors, which do not increase cAMP concentrations, and adenylate cyclase was found to be prostaglandin E2.

Animals↗
PubMed1988

Intestinal absorption of cephalosporin antibiotics: correlation between intestinal absorption and brush-border membrane transport.

The absorption of seven cephalosporin antibiotics from the in-situ intestinal loop at pH 7.4 and their transport by brush-border membrane vesicles in the presence of an inward H+ gradient ([pH]i = 7.5, [pH]o = 6.0) were examined. A good correlation was found between the intestinal absorption rate and the initial uptake rate by brush-border membrane vesicles. The data suggest that the transport study using intestinal brush-border membrane vesicles is useful as a model system for the intestinal absorption of beta-lactam antibiotics.

Animals↗
PubMed1990

Diarrhea and intestinal invasiveness of Aeromonas strains in the removable intestinal tie rabbit model.

Twelve Aeromonas strains were tested for virulence by using the removable intestinal tie adult rabbit diarrhea model. Mortality was 50% or greater for 7 of 12 strains; 23 of 37 rabbits that died developed diarrhea before death, and 11 of 27 surviving rabbits developed diarrhea. Aeromonas bacteremia was detected in 36 of 37 (97%) animals that died, but only in 2 of 27 (7%) survivors. Death, diarrhea, and bacteremia were all strongly strain dependent. Gastrointestinal lesions varied from moderate focal enteritis to severe multifocal necrosis and hemorrhage of the ileal mucosa, often accompanied by hepatic and splenic lesions. Intestinal colonization assays performed after infection indicated that the ileum was the most heavily colonized portion of the gut and the probable site of invasion. The application of the removable intestinal tie adult rabbit diarrhea model for intestinal challenge with Aeromonas strains has shown that some isolates are capable of invading the mucosa of rabbits, causing diarrhea and bacteremia. These data suggest that such strains may be important in causing human invasive diarrhea.

Aeromonas↗
PubMed1999

Study of infectious intestinal disease in England: rates in the community, presenting to general practice, and reported to national surveillance. The Infectious Intestinal Disease Study Executive.

OBJECTIVE: To establish the incidence and aetiology of infectious intestinal disease in the community and presenting to general practitioners. Comparison with incidence and aetiology of cases reaching national laboratory based surveillance. DESIGN: Population based community cohort incidence study, general practice based incidence studies, and case linkage to national laboratory surveillance. SETTING: 70 general practices throughout England. PARTICIPANTS: 459 975 patients served by the practices. Community surveillance of 9776 randomly selected patients. MAIN OUTCOME MEASURES: Incidence of infectious intestinal disease in community and reported to general practice. RESULTS: 781 cases were identified in the community cohort, giving an incidence of 19.4/100 person years (95% confidence interval 18.1 to 20.8). 8770 cases presented to general practice (3.3/100 person years (2.94 to 3.75)). One case was reported to national surveillance for every 1.4 laboratory identifications, 6.2 stools sent for laboratory investigation, 23 cases presenting to general practice, and 136 community cases. The ratio of cases in the community to cases reaching national surveillance was lower for bacterial pathogens (salmonella 3.2:1, campylobacter 7.6:1) than for viruses (rotavirus 35:1, small round structured viruses 1562:1). There were many cases for which no organism was identified. CONCLUSIONS: Infectious intestinal disease occurs in 1 in 5 people each year, of whom 1 in 6 presents to a general practitioner. The proportion of cases not recorded by national laboratory surveillance is large and varies widely by microorganism. Ways of supplementing the national laboratory surveillance system for infectious intestinal diseases should be considered.

Adolescent↗
PubMed2005

Intestinal adaptation after massive intestinal resection.

Patients with short bowel syndrome require long term parenteral nutrition support. However, after massive intestinal resection the intestine undergoes adaptation and nutritional autonomy may be obtained. Given that the complications of parenteral nutrition may be life threatening or result in treatment failure and the need for intestinal transplantation, a more attractive option is to wean patients off nutrition support by optimising the adaptive process. The article examines the evidence that after extensive small bowel resection adaptation occurs in humans and focuses on the factors that influence adaptation and the strategies that have been used to optimise this process. The review is based on an English language Medline search with secondary references obtained from key articles. There is evidence that adaptation occurs in humans. Adaptation is a complex process that results in response to nutrient and non-nutrient stimuli. Successful and reproducible strategies to improve adaptation remain elusive despite an abundance of experimental data. Nevertheless given the low patient survival and quality of life associated with other treatments for irreversible intestinal failure it is imperative that clinical research continues into the optimisation of the adaptation.

Adaptation, Physiological↗
PubMed1987

The level of dietary protein and carbohydrate has a different effect on intestinal uptake of hexoses and lipids in rabbits with an ileal resection than in those with an intact intestinal tract.

Either high protein, low carbohydrate (HP) or low protein, high carbohydrate (LP) diets were fed for 6 weeks to rabbits with or without resection of the distal half of the small intestine. Control and resected rabbits fed HP consumed more food and gained more weight than the animals fed LP. The level of dietary protein has a different effect on intestinal transport in animals with an ileal resection than in those with an intact small intestine. With 0.5 mM glucose, the in vitro uptake in control rabbits was greater for the LP than HP diet but was unchanged in resected rabbits; uptake of 0.5 mM galactose and 3-O-methyl glucose was unaffected by HP and LP, whereas in rabbit uptake was lower in LP than HP. The uptake of 40 mM glucose was greater with the LP than HP diet in control rabbits, but lower with LP than HP in resected rabbits. In control rabbits, the uptake of aluric acid was lower on the LP than HP diet; the uptake of octanoic acid, decanoic acid, and cholesterol was unchanged; and the uptake of each fatty acid and cholesterol was greater in resected rabbits fed LP than HP. Feeding a low protein diet to animals with an ileal resection is associated with lower jejunal uptake of high concentrations of glucose, but the higher uptake of galactose and enhanced permeability to fatty acids result in superior weight gain. Thus, recommendations for alterations in dietary protein and carbohydrate levels following ileal resection must be made with the knowledge that these changes may influence intestinal transport function as well as body weight gain.

Animals↗
PubMed2004

The female intestine is more resistant than the male intestine to gut injury and inflammation when subjected to conditions associated with shock states.

Having documented that proestrus female rats are more resistant to shock-induced acute gut and hence lung injury than male rats, we tested the hypothesis that the female gut is more resistant to injury and produces less of an inflammatory response than the male gut when exposed to conditions associated with shock states (hypoxia and acidosis) utilizing the ex vivo Ussing chamber system. Ileal mucosal membranes harvested from normal male and female rats mounted in Ussing chamber systems were exposed to normoxia or 40 min of hypoxia at a normal pH (pH 7.3) or acidosis (pH 6.8). Cytokine and nitric oxide levels in the serosal compartment of the Ussing chamber were measured at the end of the 3-h experimental period to assess the immunoinflammatory response, whereas FITC-dextran (mol wt 4,300) was employed to assess barrier function. Histomorphological changes were used to quantitate gut mucosal injury. Hypoxia, acidosis, or hypoxia plus acidosis was associated with a significant increase in proinflammatory cytokine production [interleukin (IL)-6, tumor necrosis factor, and macrophage inflammatory protein (MIP)-2] by the male compared with the female intestinal segments. In contrast, the female gut manifested a higher anti-inflammatory response (nitric oxide and IL-10) and improved intestinal barrier function as well as less evidence of mucosal injury than the male intestinal segments. Administration of estradiol or the testosterone receptor antagonist, flutamide, to male rats abrogated the increase in gut injury and the increased IL-6 and MIP-2 response observed after hypoxia plus acidosis. These results suggest that gender differences in the ex vivo intestinal response to stresses, such as hypoxia and acidosis, exist and that the administration of estradiol or blockade of the testosterone receptor to male rats mitigates these gender differences.

Acidosis↗
PubMed1994

Rapid upregulation of snake intestine in response to feeding: a new model of intestinal adaptation.

Mammalian guts exhibit numerous adaptive responses to feeding. However, response magnitudes are often inconveniently modest for experimental analysis, because mammals feed often and their intestines are rarely empty. We anticipated larger responses in sit-and-wait foraging snakes, because they consume huge meals at long intervals. Hence, we studied metabolic rates, brush-border nutrient transport, and intestinal morphometrics in the rattlesnake, Crotalus cerastes, as a function of time since feeding. O2 consumption by the whole snake, a reflection of the cost of digestion and of rebuilding the starved gut, peaked after 2 days at eight times fasting values. Activities of brush-border glucose, leucine, and proline transporters peaked after 1-3 days at 5-22 times fasting values. Ratios of amino acid to glucose uptake rates peaked at 104, reflecting snakes' extreme adaptation to carnivory (a high-protein low-carbohydrate diet). Intestinal mass increased more than twofold within 1 day, primarily because of mucosal growth. After defecation, the intestine atrophied, brush-border transporters were downregulated, and O2 consumption returned to basal. These rapid and large responses reduce costs of gut maintenance during long bouts of quiescence between meals. Hence sit-and-wait foraging snakes may furnish advantageous model species for studying gut regulation and adaptation.

Adaptation, Physiological↗
PubMed1994

Expression of intestinal fatty acid binding protein in intestinal epithelial cell lines, hBRIE 380 cells.

Intestinal fatty acid binding protein (I-FABP) is a cytosolic protein present only in differentiated intestinal epithelial cells. Here we report on an intestinal cell culture system expressing I-FABP during cell differentiation and the modulation of expression by extracellular factors. An I-FABP-expressing cell line (hBRIE 380i) was generated from Berkeley rat intestinal epithelial cells (hBRIE 380). Time- and substratum-dependent changes in I-FABP mRNA expression were paralleled by changes in protein levels. Induction of I-FABP levels observed on collagen type I gels in the presence of limiting serum was prevented by insulin. When cells were grown on collagen gels containing fibronectin and laminin, a stimulation of ultrastructural characteristics of cell differentiation was observed with no further induction of I-FABP expression. The data show that I-FABP expression is limited to a differentiated population of hBRIE 380i cells and that the expression can be regulated by factors present in the extracellular matrix as well as involved in regulation of replication or metabolic state of the cell.

Animals↗
PubMed1997

Immunohistochemical localization of cysteine-rich intestinal protein in rat small intestine.

Cysteine-rich intestinal protein (CRIP) is a LIM (cysteine-rich motif of leu-11, isl-1, and mec-3 genes) domain protein with a double zinc finger motif. The protein is abundantly expressed in the intestine, peritoneal macrophages, and peripheral blood mononuclear cells. The function of CRIP is not known. The purpose of this study was to determine the cellular distribution of CRIP in rat intestine, as an initial step toward eventual determination of a function. Immunohistochemical and immunogold labeling electron microscopy using a purified polyclonal rabbit antibody to a synthetic peptide representing a zinc finger domain of rat CRIP were carried out on sections of rat duodenum. Western blotting was used to detect signal specificity of the antibodies. These immunohistochemical and electron microscopy studies showed particularly high abundance of CRIP in the cytoplasmic granules of Paneth cells of the intestine. Some evidence of CRIP expression was also found in cells of the villus tip, but abundance was less than that found in the Paneth cells. The localization of CRIP in Paneth cells and its presence in mononuclear cells suggests that CRIP may be involved in host defense mechanisms and/or tissue differentiation/remodeling processes common to these cell types.

Animals↗