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PubMed1989

Eicosanoid regulation of acute intestinal vascular permeability induced by intravenous peptidoglycan-polysaccharide polymers.

A model of rapidly developing, self-limited acute vascular permeability changes localized to the gut-associated lymphoid tissue (GALT) of the rat was used to study the role of prostaglandins (PGs), thromboxanes (Txs), and leukotrienes (LTs) in the in vivo regulation of early intestinal inflammatory events. Sprague-Dawley rats were pretreated with metabolites, enzyme inhibitors, or receptor antagonists of the arachidonic acid pathway before intravenous injection of sonicated peptidoglycan-polysaccharide polymers derived from group A streptococci (PG-APS, 5 micrograms rhamnose/g body weight). Rats were killed five minutes after PG-APS injection and were evaluated grossly for petechiae of the intestinal parenchyma and lymphoid aggregates. Indomethacin or dexamethasone increased intestinal injury by PG-APS by inducing mid-small bowel and cecal parenchymal hemorrhage. Indomethacin significantly diminished colonic lymphoid aggregate hemorrhage. PGE1, PGE2, and prostacyclin dramatically inhibited GALT hemorrhage; prostacyclin was the most potent with an effective dose of 0.1 microgram/kg. Dazmegrel, a specific Tx synthetase antagonist, significantly inhibited PG-APS-induced vascular permeability. Dazmegrel continued to diminish colonic lymphoid aggregated hemorrhage during concurrent treatment with indomethacin, which removed potential endogenous prostaglandin protection. Diethylcarbamazine, a lipoxygenase inhibitor, and FPL-55712, a LT receptor antagonist, inhibited the PG-APS-induced lesions, with FPL-55712 being more potent. LT blockade had a predominant effect on the intestinal parenchymal hemorrhage. We postulate that the normal homeostatic suppression of inflammation induced by phlogistic bacterial cell wall polymers is PG mediated, and that pathological responses are Tx and LT dependent.

Animals↗
PubMed2004

Hepcidin, the recently identified peptide that appears to regulate iron absorption.

A newly identified iron regulator, hepcidin, appears to communicate body iron status and demand for erythropoiesis to the intestine, and in turn, modulates intestinal iron absorption. Hepcidin was first purified from human blood and urine as an antimicrobial peptide and was found to be predominantly expressed in the liver. A lack of hepcidin expression has been associated with iron overload and overexpression of hepcidin results in iron-deficiency anemia in mice. In addition, hepcidin levels decrease in mice fed a low iron diet and increase in mice fed a high iron diet. These observations support the role of hepcidin as a signal that limits intestinal iron absorption. Hepcidin expression is also affected by hypoxia and inflammation and is decreased in hemochromatosis patients. Thus, the relationship between body iron status and hepcidin is altered in hemochromatosis patients. In addition, hepcidin is decreased in HFE knockout mice, which demonstrates characteristics of iron overload as in hemochromatosis patients. Hence, HFE is suggested to act as a regulator of hepcidin expression. Transcription factors, such as C/EBPalpha, are also suggested to be involved in the regulation of hepcidin gene expression. However, much remains to be investigated in the regulation of hepcidin by iron, hypoxia and inflammation.

Amino Acid Sequence↗
PubMed1992

Evaluation of intestinal clearance and faecal excretion of alpha 1-antiproteinase and immunoglobulins during Crohn's disease and ulcerative colitis.

The intestinal clearance of alpha 1-antiproteinase, monomeric IgA and IgG, and the daily fecal output of polymeric IgA and IgM were investigated in patients with inflammatory bowel diseases (inactive and active Crohn's disease, ulcerative colitis) and in a control group. The intestinal clearance of alpha 1-antiproteinase was significantly increased in all patients with inflammatory bowel diseases (p less than 0.01), irrespective of the grade of the disease. In contrast, increases in intestinal clearances of monomeric IgA and IgG were more closely related to the severity of the intestinal lesions. The associate determination of these three quantities should therefore be of interest for monitoring the degree of intestinal bowel inflammation. Faecal output of polymeric IgA was significantly increased in active intestinal disease (p less than 0.01), whereas faecal IgM levels were not. The determination of the faecal output of polymeric IgA should contribute to the assessment of the activity of inflammatory bowel diseases, and may provide insight into the activation of the mucosal immune system.

Adolescent↗
PubMed2006

New strategies for diagnosis and management of celiac disease.

Celiac disease is a gastrointestinal disorder characterized by inflammation, leading to injury to the mucosal lining of the small intestine. The inflammation occurs when gliadin, a protein found in such gluten-containing foods as wheat, rye, and barley, is ingested by genetically susceptible individuals. The mucosal damage and subsequent malabsorption of nutrients leads to various complications. Researchers estimate that more than 2 million people in the United States have celiac disease-a prevalence that is greater than was previously believed. Approximately 60,000 Americans are diagnosed annually with celiac disease. Until recently, diagnosis has been complicated by the fact that the indicators of celiac disease are nonspecific. However, because of the development of new, easy-to-administer serology tests, diagnosis has become much less complicated. After conducting a review of the literature, the authors recommend a serologic testing sequence for diagnosis of celiac disease and urge that adults and children with an assortment of symptoms be tested for this disease. Common signs and symptoms of celiac disease include anemia, arthralgia, fatigue, infertility, neuropathy, and weight loss, in addition to such gastrointestinal symptomatology as abdominal pain, anorexia, bloating, constipation, and diarrhea. The only treatment for patients with celiac disease remains a gluten-free diet.

Celiac Disease↗
PubMed1993

[Physiological function of the gastrointestinal tract and pathophysiological changes in neonatal diarrhea of calves].

Firstly, the basic principles of absorption and secretion in the intestine of healthy animals are described. The etiology and the pathophysiologic mechanisms of neonatal diarrhea in the calf due to E. coli and rota-/coronavirus are discussed. Enterotoxins of E. coli stimulate primarily the secretion of chloride (and thereby water) in the small intestine without damaging the intestinal mucosa. The sodium-dependent transport systems for the absorption of glucose and amino acids remain intact. In contrast, infections with rota- or coronavirus lead primarily to a disturbance of absorption processes in the intestine due to villous atrophy. Crypt cells are indirectly affected by inflammation mediators. Intestinal motility is inhibited during most diarrheic episodes; the application of para-sympatholytics in therefore not favourable.

Animals↗
PubMed1987

Intestinal iron absorption during turpentine sterile inflammation in the rat. Influences of isoproterenol and propranolol.

59Fe was incorporated in vivo into intestinal sacs prepared in control rats as well as in animals with turpentine sterile abscesses and 59Fe counts were detected in the intestinal wall, in blood, in liver, in spleen and in femur of animals, at different time intervals (20, 40 and 120 min) following i.v. injection of isoproterenol (10 micrograms/kg, body weight) or of (-)-propranolol (2 mg/kg, body weight). In rats without inflammation isoproterenol alone enhanced significantly iron counts in blood, spleen, liver and femur, but not in intestinal cells, whereas propranolol evoked opposite actions, the influence being more marked after 40 min, reaching maximal values at 120 min. In animals with sterile turpentine abscesses explored 40 min after injections, iron intestinal counts in turpentine, in turpentine plus isoproterenol and in turpentine plus propranolol groups were significantly lower than in normal saline injected controls (p less than 0.001) and the opposite was the case at 120 min. In blood, iron counts at 20 and 40 min were higher in saline controls (p less than 0.05) than in the turpentine group, whereas at 120 min, values in the turpentine plus isoproterenol group were higher than (p less than 0.01) in saline injected controls or in the group with turpentine alone. Also, at all time intervals explored, iron counts in blood in the propranolol plus turpentine group were smaller (p less than 0.01) than in saline injected controls or in the group with turpentine alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1996

Substance P activation of enteric neurons in response to intraluminal Clostridium difficile toxin A in the rat ileum.

BACKGROUND & AIMS: Nerves have been suggested to mediate the effects of bacterial toxins in intestinal diseases. However, the mechanisms involved are unknown. This study examined endogenous substance P (SP) activation of the substance P receptor (SPR) on enteric neurons in the rat ileum after exposure to intraluminal Clostridium difficile toxin A. METHODS: After intraluminal injection of toxin A in ileal loops, tissue was examined for pathological changes by histology and for SPR activation by immunocytochemical analysis of SP-induced SPR endocytosis. RESULTS: After toxin A administration, > 70% of enteric neurons showed SPR endocytosis and became swollen with thickened dendrites. In contrast, SPRs in control rats were largely confined to the plasma membrane. Rats denervated of primary afferent fibers with neonatal capsaicin injection and animals pretreated with a nonpeptide SPR antagonist showed few endosomal SPRs, and the pathological inflammatory effects of toxin A were ablated. CONCLUSIONS: Intraluminal toxin A causes the release of SP from primary afferent neurons: this endogenous SP then acts on enteric neurons in the submucosal and myenteric plexuses. SP is the primary mediator of an axon reflex mediating neurogenic inflammation in the intestine. SPR blockade may prove to be a novel therapy used to prevent intestinal inflammation.

Animals↗
PubMed2006

Gastric carditis: Is it a histological response to high concentrations of luminal nitric oxide?

During the last decade, inflammation (carditis) and intestinal metaplasia localized to immediately below the human gastro-oesophageal junction have received much attention in relation to the rising incidence of cancer at this site. Since these histological findings are frequently observed even among those who are H pylori-negative, the causative factors for such histologic events at the human gastro-oesophageal junction remain obscure. A series of recent studies have demonstrated that a high level of salivary nitrite is sustained over several hours after the ingestion of a high nitrate meal, and that the nitrite in swallowed saliva is rapidly converted to nitric oxide by an acid catalyzed chemical reaction at the gastro-oesophageal junction. Eventually, a substantial amount of nitric oxide diffuses from the lumen into the adjacent tissue. Therefore, the human gastro-oesophageal junction is likely to be a region of high nitrosative stress. Considering the life-time exposure of the gastro-oesophageal junction to cytotoxic levels of nitric oxide, this may account for the high prevalence of inflammation, intestinal metaplasia, and subsequent development of neoplasia at this site. Although gastric acid, pepsin, and bile acid have been intensively investigated as a cause of adenocarcinoma at the gastro-oesophageal junction and the distal esophagus, nitric oxide and the related nitrosative stress should also be examined.

Adenocarcinoma↗
PubMed2003

The two faces of IKK and NF-kappaB inhibition: prevention of systemic inflammation but increased local injury following intestinal ischemia-reperfusion.

We studied the role of NF-kappaB in acute inflammation caused by gut ischemia-reperfusion through selective ablation of IkappaB kinase (IKK)-beta, the catalytic subunit of IKK that is essential for NF-kappaB activation. Ablation of IKK-beta in enterocytes prevented the systemic inflammatory response, which culminates in multiple organ dysfunction syndrome (MODS) that is normally triggered by gut ischemia-reperfusion. IKK-beta removal from enterocytes, however, also resulted in severe apoptotic damage to the reperfused intestinal mucosa. These results show the dual function of the NF-kappaB system, which is responsible for both tissue protection and systemic inflammation, and underscore the caution that should be exerted in using NF-kappaB and IKK inhibitors.

Animals↗
PubMed1997

Beneficial effects of growth hormone combined with parenteral nutrition in the management of inflammatory bowel disease: an experimental study.

BACKGROUND: Growth hormone (GH) improves net protein anabolism and stimulates wound healing. Although GH is also known to exert the trophic effect on the intestinal tract, its role in the healing of intestinal ulceration is not known. The aim of this study was to evaluate the effects of exogenous GH coinfused with parenteral nutrition (PN) in an experimental model of inflammatory bowel disease in rats. METHODS: All rats underwent central venous cannulation and were randomized to two groups after induction of small intestinal ulceration with indomethacin. Both groups received the same PN formula. In addition, the GH group (n = 10) received subcutaneous injections of human GH at a dose of 1.0 IU/kg daily for 4 days, whereas the control group (n = 10) received injections of normal saline solution. Nitrogen balance, macroscopic inflammation score, intestinal myeloperoxidase activity, DNA content, and mucosal permeability were determined for each rat. Insulin-like growth factor-I (IGF-I) mRNA was detected by reverse transcription and polymerase chain reaction. RESULTS: Administration of GH significantly improved the cumulative nitrogen balance, ameliorated the gross inflammation score, and decreased intestinal myeloperoxidase activity. Similarly, intestinal permeability was significantly decreased in the GH group as compared with the control group. GH treatment resulted in increased plasma concentration of IGF-I and IGF-I mRNA expressions in both the liver and the small intestine compared with those in the control group. CONCLUSIONS: Exogenous GH plays an important role in accelerating intestinal healing in an experimental model of small bowel ulceration in rats. The mechanisms may include the stimulated IGF-I production, which thereafter augments intestinal epithelial cell growth.

Animals↗
PubMed1977

Protection of the skin around intestinal fistulas.

The use of two recently introduced skin protective preparations in the treatment of perifistular skin inflammation is described. Karaya gum in paste form (karaya paste) and a compressed wafer of gelatin, pectin and methyl cellulose (Stomahesive) were used, alone or in combination; with drainable collecting appliances. The method protects the inflamed skin from fistula discharge and allows healing to proceed beneath the dressing. A technique to improve the adhesion of the appliance, in spite of large fluid losses, is outlined. Healing of skin excoriation was obtained in nearly all cases. Complete control of leakage was achieved in a group of patients with a high output fistula.

Administration, Topical↗
PubMed2002

No support for endoscopic surveillance for gastric cancer in hereditary non-polyposis colorectal cancer.

BACKGROUND: The DNA mismatch repair gene mutations underlying hereditary non-polyposis colorectal cancer syndrome (HNPCC) also predispose, besides colorectal and endometrial cancer, to gastric cancer. usually of the intestinal type. The carcinogenetic pathway behind the elevated gastric cancer risk is largely unknown. METHODS: The aim of this study was to determine whether there are any premalignant lesions to search for in gastric surveillance in HNPCC by comparing gastric histopathology between mutation-positive and mutation-negative family members. We searched for differences in occurrence of Helicobacter pylori, inflammation, atrophy, intestinal metaplasia and dysplastic changes. Upper gastrointestinal endoscopy was performed for 73 mutation-positive and 32 mutation-negative family members. RESULTS: One case of duodenal cancer was detected in the mutation-positive group, but no gastric neoplastic lesions were seen in either group. There were no differences in the occurrence of polyps, H. pylori, inflammation, activity, atrophy nor intestinal metaplasia tested with binaric, logistic, regression analysis. CONCLUSIONS: We conclude that surveillance gastroscopy may not be beneficial in HNPCC, since neither cases of early cancer nor premalignant lesions could be detected in our series of 73 mutation-positive subjects.

Adult↗
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↗