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PubMed2005

Animal models of intestinal inflammation: ineffective communication between coalition members.

The microbiota, epithelial cells, and mucosal immune cells in the intestine comprise an important gastrointestinal coalition. The intestinal microbiota can exert both beneficial as well as deleterious effects on their animal hosts. They interact with the innate defenses provided by epithelial cells through microbial recognition receptors. This communication, under normal conditions, results in a state of controlled inflammation. This article will focus on several animal models of intestinal inflammation, in which spontaneous or induced mutations or other genetic manipulations result in severe alterations in one of the members of the gastrointestinal coalition. These animal models of colitis have shown that alterations in communication between members of this coalition ultimately lead to gastrointestinal disease.

Animals↗
PubMed1992

Metronidazole reduces intestinal inflammation and blood loss in non-steroidal anti-inflammatory drug induced enteropathy.

This study assessed the effect of metronidazole on the gastroduodenal mucosa, intestinal permeability, blood loss, and inflammation in patients on non-steroidal anti-inflammatory drugs (NSAIDs). Thirteen patients were studied before and after 2-12 weeks' treatment with metronidazole 800 mg/day, while maintaining an unchanged NSAID intake. Intestinal inflammation, as assessed by the faecal excretion of indium-111 labelled neutrophils, and blood loss, assessed with chromium-51 labelled red cells, were significantly reduced after treatment (mean (SD) 111In excretion 4.7 (4.7)% v 1.5 (1.3)% (N < 1.0%), p < 0.001, 51Cr red cells loss 2.6 (1.6) ml/day v 0.9 (0.5) ml/day (N < 1.0 ml/day), p < 0.01). Intestinal permeability assessed as the 5 hour urinary excretion ratio of 51CrEDTA/L-rhamnose did not change significantly (0.133 (0.046) v 0.154 (0.064), p > 0.1) and there were no significant changes in the endoscopic or microscopic appearances of the gastroduodenal mucosa. These results suggest that the neutrophil is the main damaging effector cell in NSAID induced enteropathy. The main neutrophil chemo-attractant in this enteropathy may be a metronidazole sensitive microbe.

Aged↗
PubMed2005

Epithelium-specific glutathione peroxidase, Gpx2, is involved in the prevention of intestinal inflammation in selenium-deficient mice.

Mice deficient in 2 intracellular selenium (Se)-dependent glutathione peroxidases (Gpx1 and Gpx2), by genetically disrupting both alleles of the Gpx1 and Gpx2 genes (Gpx1(-/-)Gpx2(-/-)), develop ileocolitis around weaning. However, decreased Gpx activity in Se-depleted wild-type animals does not produce pathology in the gastrointestinal tract. Because a small percentage of Se-sufficient Gpx1(+/-)Gpx2(-/-) mice have mild ileocolitis, we hypothesized that Se-deficient Gpx1(+/-)Gpx2(-/-) mice will develop severe ileocolitis similarly to the Gpx1(-/-)Gpx2(-/-) mice, and even a trace amount of Gpx2 can protect intestinal mucosa against inflammation. To test our hypothesis, we fed mice at various stages of development with either Gpx1(+/)(-)Gpx2(-/-) or Gpx1(-/-)Gpx2(+/)(-) genotypes an Se-deficient diet for 4-5 wk and assessed the symptoms and pathology. Gpx1(+/)(-)Gpx2(-/-) mice that were deprived of Se in utero or at weaning (18-22 d of age), but not as young adults (31-51 d of age), manifested significantly worse pathology than their Se-sufficient counterparts. Both Gpx1 and Gpx2 activities and mRNA levels were significantly depressed in the ileum of Se-deprived mice. In mice deprived in utero, the pathology included acute inflammation with neutrophil and monocyte infiltration particularly in the colon and was externally manifested by perianal alopecia and ulceration. On the other hand, Gpx1(-/-)Gpx2(+/)(-) mice were unaffected by Se deprivation, regardless of the age of onset. The results show that a trace amount of Gpx2 is protective against ileocolitis, and Se-deficient young Gpx1(+/-)Gpx2(-/-) mice will develop pathology and symptoms similar to Se-adequate Gpx1(-/-)Gpx2(-/-) mice.

Animals↗
PubMedDate not supplied

Congenital diarrhea with intestinal inflammation and epithelial immaturity.

We report an interesting case of congenital inflammatory bowel disease and intestinal epithelial immaturity that presented as secretory diarrhea. No infectious, metabolic, or anatomical basis for these findings was identified. As differentiated from previous reports of neonatal enteropathies, this infant demonstrated involvement of both the small and large intestine with histopathologic findings of acute and chronic inflammation, extensive submucosal fibrosis, and "flat" small intestine mucosa. In addition, this patient had a polyamine deficiency (a primary or secondary phenomenon), which may have contributed to delayed epithelial maturation. These findings suggest that the inflammatory bowel disease and altered epithelial maturation contributed to a fatal intractable diarrhea.

Diarrhea, Infantile↗
PubMed2004

The expression and role of Fas ligand in intestinal inflammation.

Fas ligand (FasL) is involved in the pathogenesis of inflammatory diseases and immune privilege. We examined the expression of FasL in the enteric nervous system (ENS) in murine colitis and guinea-pig ileitis. We studied FasL immunoreactivity, functional integrity of the ENS, severity of colitis, and distribution of neutrophils in wild type and B6/gld mice that lack functional FasL. In ileitis, the distribution of FasL, CD4+ and CD8+ T cells was examined. FasL expression was increased in the ENS of wild type mice with colitis, but decreased labelling of nerve fibres was noted in B6/gld mice. Neutrophils were more abundant and widely distributed in B6/gld mice. Colitis was more severe and persistent in B6/gld mice 7 days after induction. Functional parameters of intestinal secretion and motility in B6/gld mice were the same as controls. In ileitis, FasL expression was increased in the guinea-pig ENS and returned to control levels following the resolution of inflammation. While T cells were not present in the ENS of controls, they were observed during inflammation, but were excluded from ganglia. The number of enteric neurons was unchanged over the course of inflammation. The expression of FasL is altered in intestinal inflammation and contributes to its resolution in experimental colitis.

Animals↗
PubMed2006

Toll-like receptor signaling and its relevance to intestinal inflammation.

This review discusses the current progress in the understanding of how commensal-mediated activation of toll-like receptors (TLRs) may be involved in the regulation of physiological and pathophysiological processes of the intestinal mucosa including tissue regeneration and inflammation. While regulation of TLRs and their downstream signaling mediators might be used to prevent and treat inflammatory bowel diseases, paradoxically, at this time, it remains uncertain whether this would be more effectively accomplished by enhancing or inhibiting these pathways.

Animals↗
PubMed1995

Intestinal inflammation associated with flagellates in snakes.

The intestines of 51 snakes with histologically diagnosed or suspected amoebiasis were reinvestigated immunohistochemically with an Entamoeba invadens antibody. In 22 cases, trophozoites of Entamoeba invadens stained positively in the inflamed intestinal wall, but the protozoa visible in the pathologically changed intestines of a further 20 snakes were negative. On the basis of light and electron microscopical findings, these protozoa were identified as flagellates.

Animals↗
PubMed1983

Peritoneal cell responses to acute gastro-intestinal inflammation.

Cell changes in the peritoneal exudate induced by an acute localised inflammation due to a small intestinal anastomosis have been studied. The maximum response occurs on the second day. The neutrophil polymorphonuclear leucocyte output on the second is seven times greater in the peritoneal exudate than in the effluent lymph from the gastro-intestinal tract. The fate of the inflammatory cell response of the peritoneal exudate has been studied using thymidine-labelled cell transfer experiments. Some neutrophil polymorphonuclear leucocytes and eosinophils are phagocytosed by monocyte/macrophage cells in the peritoneal cavity. The majority of the neutrophil polymorphonuclear leucocytes and eosinophils migrate through diaphragmatic "stomata" to the parathymic lymph glands via the mediastinal lymphatics.

Acute Disease↗
PubMed2002

Role of tumor necrosis factor receptor 2 (TNFR2) in colonic epithelial hyperplasia and chronic intestinal inflammation in mice.

BACKGROUND & AIMS: Tumor necrosis factor (TNF) induces multiple effects including cell proliferation and death by ligation with TNF receptor type II (TNFR2). We studied the role of TNFR2 in chronic inflammation-induced colonic epithelial alteration. METHODS: TNFR2 expression in colonic epithelial cells (CECs) was assessed by ribonuclease protection assay (RPA) and immunohistochemistry (IHC) in patients with inflammatory bowel disease (IBD) and murine colitis models. TNFR2 expression was also analyzed using COLO205 cells. The role of TNFR2 in colonic epithelial homeostasis was examined by generating interleukin 6-deficient TCR alpha KO (alpha IL-6DKO) or TNFR2-deficient TCR alpha (alpha TNFR2DKO) mice. RESULTS: TNFR2 expression was up-regulated in CEC in both human ulcerative colitis and Crohn's disease. In vitro studies showed that TNFR2 expression was up-regulated by a cooperative effect of key proinflammatory cytokines. By RPA, the increased expression of TNFR2 was detectable in TCR alpha KO mice with colitis compared with TCR alpha KO mice without colitis or wild-type mice. In alpha IL-6DKO mice, TNFR2 expression, proliferation, and nuclear factor kappa B activation of CECs were markedly reduced compared with TCR alpha KO mice. alpha TNFR2 mice also showed significantly less colonic epithelial proliferation compared with TCR alpha KO mice. CONCLUSIONS: Expression of TNFR2 is consistently increased on CECs in both murine colitis models as well as patients with IBD. TNFR2 may play an important role in colonic inflammation-associated alteration in the intestinal epithelium.

Animals↗
PubMed1995

Spontaneous intestinal inflammation and nitric oxide metabolism in HLA-B27 transgenic rats.

BACKGROUND & AIMS: It has been reported that transgenic rats expressing the HLA-B27 and the beta 2- microglobulin genes develop spontaneous gastrointestinal (GI) inflammation; however, no systematic or quantitative evaluation of this GI inflammation has been reported. Therefore, the objective of this study was to characterize quantitatively the GI injury and inflammation observed in commercially available HLA-B27 transgenic rats. METHODS: HLA-B27 rats and Fisher 344 male controls were used for these studies. Gastric, ileal, and colonic blood-to-lumen clearances of 51Cr-ethylenediaminetetraacetic acid, tissue myeloperoxidase activities, and wet/dry ratios of the various tissues as well as plasma nitrate and nitrite levels were quantified for each control and transgenic animal. RESULTS: Spontaneous ileitis and colitis developed in 5 of 10 HLA-B27 transgenic rats beginning at approximately 17 weeks of age and persisting for an additional 13 weeks. Increases in mucosal permeability and myeloperoxidase activities as well as histological analysis showed intestinal injury and chronic inflammation. Plasma levels of nitrate and nitrite, the stable decomposition products of nitric oxide, were found to be significantly enhanced (fourfold) only in those rats that developed the intestinal inflammation. CONCLUSIONS: The chronic ileitis and colitis observed in HLA-B27 transgenic rats seems to be associated with enhanced NO metabolism.

Animals↗
PubMed2004

Induced reactivity of intestinal CD4(+) T cells with an epithelial cell lectin, galectin-4, contributes to exacerbation of intestinal inflammation.

Inflammatory bowel disease is an immune-mediated intestinal inflammatory condition that is associated with an increase in autoantibodies that bind to epithelial cells. However, it is unknown whether the epithelial cell-derived products that are recognized by such autoantibodies are involved in the pathogenic process. Through a combined antigen-screening approach utilizing humoral and cellular immune responses, we identify herein an epithelial lectin, galectin-4, that specifically stimulates IL-6 production by CD4(+) T cells. Interestingly, the reactivity of CD4(+) T cells to galectin-4 is precisely elicited under intestinal inflammatory conditions. The galectin-4-mediated production of IL-6 is MHC class II independent and induced by PKCtheta-associated pathway through the immunological synapse. The galectin-4-mediated stimulation of CD4(+) T cells is shown to exacerbate chronic colitis and delay the recovery from acute intestinal injury. These studies identify the presence of an immunogenic, endogenous lectin in the intestine and dissect the biological role of lectin/CD4(+) T cell interactions under inflammatory conditions.

Animals↗
PubMedDate not supplied

Total parenteral nutrition alters molecular and cellular indices of intestinal inflammation in neonatal piglets.

BACKGROUND: The adverse effects of TPN on systemic immunity are well-documented; however, the impact of IV feeding on neonatal intestinal immunity is unknown. METHODS: A piglet TPN model was used to compare immune cell composition within the intestinal epithelium and lamina propria of parenterally and orally fed piglets. RESULTS: Small intestinal weight of piglets maintained intravenously was reduced 50% after 7 days. Intestinal atrophy in piglets fed parenterally was evidenced by decreased width of intestinal villi and colon cuffs and reduced intestinal crypt depth. The numbers of CD4+ and CD8+ T lymphocytes were threefold greater within the lamina propria of jejunal and ileal villi of piglets supported intravenously. Inverse correlations were observed between villus height or width and T-lymphocyte numbers (r = -.80; p < .05). Major histocompatibility complex class II mRNA expression, an indicator of localized inflammation, was increased in the ileum and colon of piglets receiving parenteral nutrition. Goblet cell numbers were two-fold greater in jejunal and ileal villi, and mast cells were more abundant in the colon of piglets fed parenterally. Furthermore, jejunal T-lymphocyte numbers were correlated with goblet cell numbers (r = .80; p = .01). CONCLUSIONS: These data identify molecular and cellular indices of intestinal inflammation that are responsive to IV feeding in neonates and provide a novel framework to investigate mechanisms underlying gut atrophy during TPN.

Animals↗
PubMed1993

Mechanisms of acute and chronic intestinal inflammation induced by indomethacin.

The objective of this study was to characterize the mechanisms of acute and chronic intestinal mucosal injury and inflammation induced by subcutaneously injected indomethacin (Indo). One injection of Indo (7.5 mg/kg) produced acute injury and inflammation in the distal jejunum and proximal ileum that were maximal at three days and completely resolved within one week. Two daily subcutaneous injections of Indo produced a more extensive and chronic inflammation that lasted in an active form in more than 75% of the rats for at least two weeks. Epithelial injury, as measured by enhanced mucosal permeability, was significantly elevated only at one day in the acute model (one injection) but was persistently elevated in the chronic model (two injections). Bile duct ligation completely attenuated increased mucosal permeability in the acute model, however, depletion of circulating neutrophils had no effect. Neither Indo (0-0.1 mg/ml) nor normal bile was cytotoxic to cultured rat intestinal epithelial cells; however, they synergistically promoted significant cytotoxicity. Bile collected from rats treated with Indo was cytotoxic towards the epithelial cells in a dose-dependent manner. Sulfasalazine and metronidazole (100 mg/kg/day, both) attenuated enhanced mucosal permeability in the chronic model. Massive bacterial translocation into the mesenteric lymph nodes, liver, and spleen following two injections of Indo was significantly attenuated by metronidazole. We conclude that: (1) a single injection of Indo produces acute intestinal mucosal injury and inflammation that resolve completely within three to seven days, whereas two daily injections of Indo produce both acute and chronic injury and inflammation, (2) enterohepatic circulation of Indo is important in promoting the acute phases of injury and inflammation, (3) circulating neutrophils do not play a role in the pathogenesis of this model, and (4) endogenous bacteria play an important role in exacerbating and/or perpetuating the chronic phases of injury and inflammation.

Acute Disease↗
PubMed2005

Growth hormone reduces the severity of fibrosis associated with chronic intestinal inflammation.

BACKGROUND & AIMS: Growth hormone (GH) is used to treat growth delay in children with Crohn's disease and in patients with short-bowel syndrome. GH can increase collagen accumulation in intestinal mesenchymal cells, raising concern that GH therapy could exacerbate fibrosis in patients with Crohn's disease. We tested if GH treatment altered inflammation or fibrosis during chronic, experimental granulomatous enterocolitis. METHODS: Ileum and cecum of Lewis rats were subserosally injected with peptidoglycan-polysaccharide (PG-APS) or control human serum albumin. At the onset of chronic PG-APS-induced inflammation, rats were administered recombinant human GH or vehicle for 14 days. Fibrosis and inflammation were quantified by gross gut disease scoring, histologic scoring, type I collagen, and cytokine expression in cecum. Abundance and localization of suppressor of cytokine signaling-3 (SOCS-3) messenger RNA and/or protein were determined in cecum. Effect of GH, cytokines, or PG-APS on SOCS-3 synthesis was measured in intestinal myofibroblasts. Myofibroblasts overexpressing SOCS-3 were used to test whether SOCS-3 inhibits collagen accumulation. RESULTS: In PG-APS-injected rats, GH modestly reduced gross adhesions and mesenteric contractions, cecal fibrosis score, and collagen expression, but had no effect on intestinal inflammation. GH increased SOCS-3 messenger RNA and protein abundance in PG-APS rats and SOCS-3 messenger RNA was localized to the periphery of granulomas. GH in combination with cytokines or PG-APS, but not alone, induced SOCS-3 synthesis in intestinal myofibroblasts. Myofibroblasts overexpressing SOCS-3 showed reduced cytokine-induced collagen accumulation. CONCLUSIONS: GH modestly reduces intestinal fibrosis associated with chronic experimental enterocolitis and stimulates expression of antifibrogenic SOCS-3, suggesting that GH therapy in inflammatory bowel disease should not exacerbate fibrosis.

Animals↗
PubMed1990

[Chronic nonspecific intestinal inflammations in older patients and their surgical treatment].

The author describes his experience with the treatment of chronic non-specific inflammations of the small and large intestine in elderly patients. They are difficult to diagnose as they are less frequent at that age. They are operated late, only when there are already serious complications (peritonitis, toxic megacolon, intractable haemorrhage and septicaemia) and the mortality is high. The author recommends therefore to pay more attention to this condition in advanced age groups.

Age Factors↗
PubMed2003

Role of the CD5 molecule on TCR gammadelta T cell-mediated immune functions: development of germinal centers and chronic intestinal inflammation.

Although CD4(+) T cells form a major subset of TCRalphabeta T cells, only a small number of TCRgammadelta T cells express CD4. Factors contributing to the down-regulation of CD4(+) TCRgammadelta T cells have not been identified. The CD5 molecule is expressed on most TCRgammadelta T cells in the spleen, whereas only a few intestinal intraepithelial TCRgammadelta T cells express this molecule in wild-type mice and TCRbeta mutant (beta(-/-)) mice. Unexpectedly, in the present studies, the lack of CD5 led to a remarkable increase of a CD4(+) TCRgammadelta T cell subset in CD5(-/-)beta(-/-) mice. The CD4(+) TCRgammadelta T cells were also detectable in MHC II(-/-)CD5(-/-)beta(-/-) triple-mutant mice. This CD4(+) TCRgammadelta T cell subset provided help in Mycobacterium-induced germinal center (GC) formation and showed a T(h)-like cytokine profile. In contrast, CD5(+) TCRgammadelta T cells suppressed the CD4(+) TCRgammadelta T cell-mediated GC formation, presumably by eliminating this CD4(+) subset. Unlike intraepithelial gammadelta T cells, >30% of TCRgammadelta T cells in the colonic lamina propria (LP) expressed CD5. The lack of CD5 also led to increased numbers of CD4(+) TCRgammadelta T cells in the colonic LP and increased susceptibility to development of chronic colitis in beta(-/-) mice. Cell transfer studies suggest that CD5(+) TCRgammadelta T cells are capable of selectively eliminating CD4(+) TCRgammadelta T cells in the intestine. The CD4(+) TCRgammadelta T cells possess immune functions similar to CD4(+) TCRalphabeta T cells.

Animals↗
PubMed1993

Regional content of enteric substance P and vasoactive intestinal peptide during intestinal inflammation in the parasitized ferret.

Our aim was to characterize and quantitate changes in two key neuropeptides, substance P (SP) and vasoactive intestinal peptide (VIP), that are involved in governing neurally-mediated gastrointestinal (GI) reflex activity during enteric inflammation in the ferret. Neuropeptide content was determined by radioimmunoassay of extracts of jejunal, ileal and colonic muscularis externa from uninfected ferrets and ferrets infected with enteric stages of the parasitic nematode, Trichinella spiralis. Increased myeloperoxidase activity (MPO), an enzymatic marker of inflammation, occurred in all three gut regions. Histopathological changes were present only in the small intestine. Significant reductions were detected in both SP (72% decrease) and VIP (62% decrease) in the inflamed jejunum. Ileal concentrations of both SP (77% decrease) and VIP (46% decrease) were also decreased during T. spiralis infection compared to uninfected ferrets. Only SP (58% decrease) concentration showed a significant change in colonic tissues from infected ferrets; colonic VIP was unaltered. Parasite-induced inflammation caused significant changes in peptide-containing enteric neural pathways and might contribute to functional GI motor disturbances that occur during nematode infections in mammalian hosts.

Animals↗