Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Intestinal Inflammation”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources
PubMed2006

Endocannabinoid overactivity and intestinal inflammation.

Cannabinoid receptors of type 1 and 2 (CB(1) and CB(2)), endogenous ligands that activate them (endocannabinoids), and mechanisms for endocannabinoid biosynthesis and inactivation have been identified in the gastrointestinal system. Activation of CB(1 )receptors by endocannabinoids produces relaxation of the lower oesophageal sphincter and inhibition of gastric acid secretion, intestinal motility, and fluid stimulated secretion. However, stimulation of cannabinoid receptors impacts on gastrointestinal functions in several other ways. Recent data indicate that the endocannabinoid system in the small intestine and colon becomes over stimulated during inflammation in both animal models and human inflammatory disorders. The pathological significance of this "endocannabinoid overactivity" and its possible exploitation for therapeutic purposes are discussed here.

Cannabinoid Receptor Modulators↗
PubMed1987

Changes in the medulla of the parathymic lymph nodes of the rat during acute gastro-intestinal inflammation.

The changes occurring in the medullary sinus and medullary cord of the parathymic lymph nodes were studied in rats after performing a small intestinal anastomosis. Polymorphonuclear leucocytes and eosinophils were phagocytosed by the macrophages of the medullary sinus. The sinus macrophages stained strongly for acid phosphatase and weakly for non-specific esterase. The medullary sinus macrophages were most numerous near the subcapsular sinus. After a small intestinal anastomosis the sinus macrophages increased in size and in number. The macrophages of the medullary cord differed from those of the medullary sinus both histochemically and ultrastructurally. The cord macrophages stained weakly for acid phosphatase, stained strongly for non-specific esterase and phagocytosed plasma cells, particularly in those specimens 2 and 5 days after the intestinal anastomosis. There was an initial significant decrease in IgA plasma cells at 2 days after the anastomosis but a subsequent increase in IgG and IgM plasma cells. The increase in IgM plasma cells preceded that of the other plasma cells.

Animals↗
PubMed1999

A role for the hepatobiliary system in IgE-mediated intestinal inflammation in the rat.

BACKGROUND: For many years the central focus of research into gastrointestinal hypersensitivity reactions has been the mast cell population of the intestinal lamina propria. Since bile is known to deliver immunological mediators to the gastrointestinal tract, the possibility arises that extra-intestinal populations of mast cells may also contribute to IgE-mediated intestinal damage. OBJECTIVES: To characterize hepatic mast cells in the rat and to investigate the role of the hepatobiliary system in a model of IgE-mediated reactivity to dietary antigen. METHODS: Wistar rats were passively sensitized with monoclonal antidinitrophenyl (DNP) IgE antibodies, and were later challenged orogastrically with DNP-HSA. Additional animals were sensitized, then bile duct-cannulated prior to antigen challenge. At various time points, liver and intestinal samples were collected for histological examination, and bile was collected and assayed for histamine and TNFalpha. RESULTS: Hepatic mast cells display a mucosal mast cell-like phenotype, and are closely associated with the vessels of the portal triads. Orogastric antigen challenge led to a rapid and significant decline (P<0.0001) in detectable mast cells as a result of anaphylactic degranulation. The median number of granulated mast cells associated with each portal triad in liver sections declined from six per portal triad to one per portal triad post-antigen challenge. After 15 min, biliary histamine concentrations rose above background levels (P<0.01). TNFalpha was also detectable in the majority (4/6) of bile samples within 15 min of challenge. Histological examination of the gastrointestinal mucosa revealed disruption to the villous epithelium ranging from oedematous changes to gross destruction. Such damage was not seen in animals in which bile had been externally drained. CONCLUSION: The data indicate that biliary products are major contributors to the gastrointestinal damage arising from IgE-mediated hypersensitivity reactions in the rat, and such hypersensitivity reactions may involve a population of mast cells which reside in the liver.

Animals↗
PubMedDate not supplied

Attenuation of Helicobacter pylori endotoxin-provoked rat intestinal inflammation by selective inhibition of the inducible nitric oxide synthase.

We studied the actions of purified Helicobacter pylori endotoxin (3 mg kg(-1), i.v.) on rat intestinal vascular permeability (assessed by the radiolabelled human serum albumin leakage technique) and on nitric oxide synthase induction (assessed by the citrulline assay) 4 h later. We found increased albumin leakage and expression of the inducible nitric oxide synthase in jejunum and colon, effects reversed by a selective inducible nitric oxide synthase inhibitor N-(8-(aminomethyl)benzyl)-acetamidine (1400W; 0.2-1 mg kg(-1), s.c., concurrently with endotoxin). Thus, H. pylori endotoxin seems to be capable of provoking an inflammatory response in the rat intestinal tissue. Systemic liberation of H. pylori endotoxin might possibly attenuate jejunal and colonic mucosal barrier function, a process mediated by the expression of the inducible nitric oxide synthase.

Amidines↗
PubMed2003

Lack of interleukin-10 leads to intestinal inflammation, independent of the time at which luminal microbial colonization occurs.

Previous studies have demonstrated that the resident bacteria harbored by interleukin (IL)-10 gene-deficient mice initiate an enterocolitis in the neonatal period. The associated intestinal injury is characterized by an increase in the secretion of interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha, and by a systemic response to endogenous bacterial antigens, supporting the hypothesis that a lack of tolerance may be the initiating cause. Whether bacterial initiation of this enterocolitis would occur in the adult intestine or whether it is only seen in the developing neonatal intestine was not known. Adult (9 weeks of age), axenic, luminally sterile IL-10 gene-deficient mice, which do not spontaneously develop enterocolitis, were inoculated with intestinal microbial flora. These mice rapidly developed intestinal injury and demonstrated elevated levels of IFN-gamma in cecal and colonic tissue. This response precedes a systemic spleen cell response to stimulation by bacterial antigens. Similarly, axenic, IL-10 gene-deficient mice exposed to microflora as neonates experience a comparable intestinal injury and IFN-gamma release before the appearance of IFN-gamma-producing cells in the spleen. Microbial colonization in control mice leads to systemic IL-10 production, but not systemic IFN-gamma production, suggesting that an IL-10-mediated suppression regulates the response in normal control mice but is absent in IL-10 gene-deficient mice. Our results suggest that the point at which intestinal microbial colonization occurs does not significantly influence the severity or specificity of the inflammatory response in IL-10 gene-deficient mice. The lack of tolerance to bacterial antigens appears to result from the absence of IL-10 during bacterial exposure.

Animals↗
PubMed2006

Correlation between cyclical epithelial barrier dysfunction and bacterial translocation in the relapses of intestinal inflammation.

BACKGROUND: Although several factors have been implicated in the pathogenesis of inflammatory bowel disease (IBD), the mechanisms underlying the recurrent relapses have not yet been clarified. We hypothesized that epithelial barrier dysfunction, associated with intestinal motor disturbances, could play a key role in exacerbation of inflammatory illness due to an increased uptake of luminal antigen and bacterial translocation. METHODS: Indomethacin administration to rats induced a long-lasting oscillation of active and quiescent phases of inflammation associated with phases of hypo and hypermotility. Rats selected at either active or quiescent phase and from 2 to 60 days after indomethacin treatment were used. Short-circuit current; conductance and HRP flux were evaluated in small intestinal segments mounted in Ussing Chambers. Enterocyte endosomes containing HRP and ultrastructural damage were assessed by electron microscopy. Bacterial translocation was determined by cultures from mesenteric lymph nodes. RESULTS: Rats with induced enteritis in both phases demonstrated a long-lasting increase of epithelial paracellular permeability. In contrast, transcellular permeability was only disturbed during the active phases, coinciding with bacterial translocation and the increase in inflammatory parameters. Furthermore, although mithochondrial damage was observed throughout the inflammatory state, alterations were worse during the active phase. CONCLUSIONS: The sustained enhancement of paracellular permeability could facilitate the constant passage of luminal antigens through the mucosa, and hence, be the basis for chronicity. By contrast, transcellular permeability only increases during the active phases, when hypomotility and bacterial translocation are also present, suggesting this factor may play a critical role in the course of acute relapses in IBD.

Animals↗
PubMedDate not supplied

Neither intact nor hydrolyzed soy proteins elicit intestinal inflammation in neonatal piglets.

BACKGROUND: Efficacy of feeding hydrolyzed soy proteins to infants intolerant to cow milk proteins has not been determined fully. This study compared growth and intestinal responses of neonatal piglets fed formulas with hydrolyzed soy protein to piglets fed formulas with intact soy or cow milk (casein-whey) proteins. METHODS: Piglets (n = 40, day 2 postpartum) were fed commercial milk replacer until day 7 postpartum (designated day 0) and then were assigned randomly to casein-whey (CW) or soy (intact, SI; hydrolyzed SH) formulas to evaluate intestinal responses on days 0, 2, 5, and 10. RESULTS: Average daily gain was higher for CW (121 g/d; p < .05) compared with SI piglets 85 g/d); SH pig weight gain was intermediate (109 g/d). Villus height-to-crypt depth ratio in proximal jejunum was lower (p < .05) on day 2 than day 0 in soy-fed pigs and lower (p < .05) on day 5 than day 0 in CW pigs. Mucosal mast cells were generally higher in CW pigs compared with soy-fed pigs. Villus goblet cell numbers in the midjejunum of SH-fed piglets were lower (p < .05) on day 5 compared with day 0. On day 5, crypt goblet cell numbers were higher (p < .05) in the midjejunum of CW-fed piglets compared with SH-fed piglets with numbers intermediate for SI-fed piglets. Intestinal differences were not detected among dietary treatments for major histocompatibility complex class I and II gene expression, tissue concentrations of prostaglandin E2, or CD8+ T-cell numbers. CONCLUSIONS: Hydrolyzed soy proteins do not elicit intestinal inflammatory responses in piglets and may be viable alternatives to milk and intact soy proteins for feeding infants.

Animal Nutritional Physiological Phenomena↗
PubMed2005

Etiology of Crohn's disease: Do certain food additives cause intestinal inflammation by molecular mimicry of mycobacterial lipids?

Crohn's disease is a chronic granulomatous inflammation of the gastrointestinal tract which was first described in the beginning of the 20th century. The histological similarity with intestinal tuberculosis has led to the assumption of an involvement of mycobacteria and mycobacterial antigens, respectively, in the etiology. A major defense mechanism against mycobacterial lipid antigens is the CD1 system which includes CD1 molecules for antigen presentation and natural killer T cells for recognition and subsequent production of cytokines like interferon-gamma and tumour necrosis factor-alpha. These cytokines promote granulomatous transformation. Various food additives, especially emulsifiants, thickeners, surface-finishing agents and contaminants like plasticizers share structural domains with mycobacterial lipids. It is therefore hypothesized, that these compounds are able to stimulate by molecular mimicry the CD1 system in the gastrointestinal mucosa and to trigger the pro-inflammatory cytokine cascade. The understanding of Crohn's disease as a CD1-mediated delayed-type hypersensitivity to certain food additives would lead to strong emphasis on a dietary treatment. Related aspects of pathology, physiology and epidemiology of Crohn's disease are presented.

Colitis↗
PubMed1998

Role of nitric oxide and platelet-activating factor in the initiation of indomethacin-provoked intestinal inflammation in rats.

The effect of indomethacin following the concurrent administration of the nitric oxide (NO) synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on acute intestinal microvascular permeability has been investigated in the rat. Administration of indomethacin (10 mg/kg, s.c.) or L-NAME (10 mg/kg, s.c.) alone did not affect jejunal and ileal vascular permeability over a 12 h period, as determined by the leakage of radiolabelled serum albumin. By contrast, when indomethacin (10 mg/kg, s.c.) was injected concurrently with L-NAME (2-10 mg/kg, s.c.) significant time-dependent plasma leakage occurred in intestinal tissues over 12 h, being apparent within 1 h. Pretreatment with L-arginine (300 mg/kg, s.c.) 15 min prior L-NAME prevented these changes in microvascular permeability. Likewise, pretreatment with the platelet-activating factor receptor antagonist, WEB 2086 ((3-[4-(2-chlorophenyl)-9-methyl-6H-thienol[3,2-f][1,2,4]triazolo- [4,3-a][1,4]diazepine-2-yl]-1-(4-morpholynil)-1-propanone), 0.1-1 mg/kg, s.c.) dose-dependently attenuated such damage. These findings suggest that following indomethacin administration, the early inhibition of NO synthase leads to acute microvascular injury involving platelet-activating factor in the rat jejunum and ileum, indicating a protective role of NO, formed by constitutive NO synthase.

Animals↗