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PubMed2003

Complement activation in plasma before and after infliximab treatment in Crohn disease.

BACKGROUND: Crohn disease is characterized by up-regulated intestinal inflammation mainly caused by increased tumour necrosis factor alpha (TNF-alpha) levels. However, the complement system (C) may also have a role in maintaining inflammation. METHODS: Plasma from 26 patients with Crohn disease complicated by fistulizing ano-rectal disease was collected before and after three Infliximab infusions (5 mg kg(-1)). RESULTS: Before treatment, the C3-activation capacities (C3-AC) in plasma from patients with Crohn disease were comparable with values obtained from healthy controls. The classical C pathway-mediated C3-AC, mannan-binding lectin C4-AC, leucocyte count, C-reactive protein concentration and Crohn Disease Activity Index decreased significantly 8 weeks after the first infusion of Infliximab (P < 0.04, Wilcoxon test). CONCLUSIONS: Before treatment, all three C pathways were within the normal range in plasma from patients with Crohn disease; the decrease observed in the classical pathway-mediated C3-AC after treatment with Infliximab reflects a general down-regulation in immune activation.

Adolescent↗
PubMed2005

Amelioration of experimental colitis by Na-H exchanger-1 inhibitor amiloride is associated with reversal of IL-1ss and ERK mitogen-activated protein kinase.

OBJECTIVE: Na-H exchanger-1 (NHE-1) is induced in experimental colitis. It has not yet been established whether its inhibition ameliorates colitis. The effects of amiloride, an inhibitor of NHE-1, on colitis were examined in this study. Levels of mitogen-activated protein (MAP) kinases ERK, p38 and interleukin 1ss which participate in intestinal inflammation were also examined in the colonic smooth muscle of rats with colitis. MATERIAL AND METHODS: Colitis was induced in Sprague-Dawley male rats by intrarectal administration of trinitrobenzenesulphonic acid (TNBS) and treated daily with amiloride (3, 5, and 10 mg/kg b.w. (body-weight), orally) starting 1 h before induction of colitis. The animals were sacrificed on day 5 post-TNBS. Controls received phosphate buffered saline in a similar manner. RESULTS: The highest dose of amiloride (10 mg/kg) was lethal. The lowest dose (3 mg/kg) was tolerated and was used in this study. Amiloride significantly reversed the colitis-reduced contractility and induction of MPO activity, NHE-1, IL-1ss and ERK, but not of p38 in inflamed colonic smooth muscle. Splenomegaly, increased colonic mass and decreased sodium pump activity were significantly reversed by amiloride treatment. There was no recovery of b.w. loss in the treated colitic animals. Urine output was increased, whereas food and water intake remained unchanged following amiloride treatment. CONCLUSIONS: These findings suggest that the beneficial effects of NHE-1 inhibition in experimental colitis are mediated through IL-1ss and ERK MAP kinase.

Amiloride↗
PubMed2005

Oral ferrous fumarate or intravenous iron sucrose for patients with inflammatory bowel disease.

OBJECTIVE: Iron therapy may reinforce intestinal inflammation by catalysing production of reactive oxygen species. The effects of oral ferrous fumarate and intravenous iron sucrose on clinical disease activity and plasma redox status were investigated in patients with inflammatory bowel disease (IBD). MATERIAL AND METHODS: Nineteen patients with iron deficiency anaemia and Crohn's disease (11) or ulcerative colitis (8) were included in a crossover study. The patients were randomly assigned to start treatment with ferrous fumarate (Neo-fer) 120 mg orally once daily or iron sucrose (Venofer) 200 mg intravenously 3 times during a period of 14 days. Clinical disease activity assessment and blood and faecal analysis were performed on days 1 and 15. RESULTS: Following oral ferrous fumarate clinical disease activity (p=0.037), general well-being score (i.e. patients felt worse) (p=0.027) and abdominal pain score (p=0.027) increased, while no changes were seen following iron sucrose treatment. C-reactive protein (CRP) and faecal calprotectin were unchanged after both treatments. As compared with iron sucrose, ferrous fumarate increased Crohn's disease activity index (CDAI) scores of general well-being (p=0.049), whereas alterations in clinical disease activity (p=0.14) and abdominal pain score (p=0.20) did not differ. Ferrous fumarate did not significantly alter plasma malondialdehyde (MDA) or plasma antioxidants. Iron sucrose increased plasma MDA (p=0.004) and decreased plasma vitamin C (p=0.017) and betacarotene (p=0.008). CONCLUSIONS: Oral ferrous fumarate, but not intravenous iron sucrose, increased clinical disease activity in IBD patients. Intravenous iron sucrose increased intravascular oxidative stress.

Administration, Oral↗
PubMed1998

Role of interleukin-10 in a murine model of dextran sulfate sodium-induced colitis.

BACKGROUND: Increased production of proinflammatory cytokines is characteristic of both animal models of experimental colitis and human inflammatory bowel disease. This study was designed to characterize the functional role of interleukin (IL)-10 in a murine model of experimental colitis. METHODS: Cytokine profiles were analyzed in animals with dextran sulfate sodium-induced colitis. The effect of treatment with IL-10 or anti-IL-10 antibodies on colonic cytokine production in vitro and tissue damage in vivo were evaluated. RESULTS: After the induction of colitis, there was a time-dependent increase in tissue tumor necrosis factor-alpha and IL-1beta levels, followed by a peak of the IL-10 level. The production of tumor necrosis factor-alpha and IL-1beta by cultured colonic tissues was inhibited by addition of IL-10, and conversely, it was enhanced by anti-IL-10. Treatment with IL-10 resulted in a marked improvement in intestinal inflammation. Blocking endogenous IL-10 was found to cause a modest exacerbation of inflammation. CONCLUSIONS: These results show that IL-10 has a functional role in regulating colonic inflammation during experimental colitis.

Animals↗
PubMed2002

Faecal calprotectin levels in infants with infantile colic, healthy infants, children with inflammatory bowel disease, children with recurrent abdominal pain and healthy children.

UNLABELLED: This study investigated faecal calprotectin concentration, a measure of intestinal inflammation, in infants and children with abdominal pain. Faecal calprotectin was measured by an enzyme-linked immunosorbent assay kit in spot stool samples in 76 infants with typical infantile colic, 7 infants with transient lactose intolerance and 27 healthy infants. All infants were 2-10 wk of age. In addition, 19 children with recurrent abdominal pain (RAP; mean age 11.5 y), 17 with inflammatory bowel disease (IBD; mean age 11.1 y; 10 had Crohn's disease and 7 ulcerative colitis) and 24 healthy children (mean age 5.3 y) were studied. In infants with infantile colic the mean faecal calprotectin concentration was not different from that in healthy infants (278 +/- 105 vs 277 +/- 109 mg kg(-1), p = 0.97) or in infants with transient lactose intolerance (300.3 +/- 124 mg kg(-1), p = 0.60). The calprotectin level was similar in boys and girls and fell significantly with age (p = 0.04). Children with IBD had faecal calprotectin levels (293 +/- 218 mg kg(-1)) much higher than healthy children (40 +/- 28 mg kg(-1), p < 0.0001) and children with RAP without identified organic disease (18 +/- 24 mg kg(-1), p < 0.0001). CONCLUSION: Faecal calprotectin may differentiate between functional abdominal pain and IBD in school-aged children. In young infants high faecal calprotectin levels are normal.

Abdominal Pain↗
PubMed1999

Hapten-induced colitis is associated with colonic patch hypertrophy and T helper cell 2-type responses.

To investigate the potential involvement of T helper (Th)2-type responses in murine models of intestinal inflammation, we used trinitrobenzene sulfonic acid (TNBS)-hapten to induce inflammatory bowel disease in situations where Th1-type responses with interferon (IFN)-gamma synthesis are either diminished or do not occur. Intracolonic administration of TNBS to either normal (IFN-gamma+/+) or Th1-deficient IFN-gamma knockout (IFN-gamma-/-) BALB/c mice resulted in significant colitis. In IFN-gamma-/- mice, crypt inflammation was more severe than in IFN-gamma+/+ mice and was accompanied by hypertrophy of colonic patches with a lymphoepithelium containing M cells and distinct B and T cell zones resembling Peyer's patches. Hapten-specific, colonic patch T cells from both mouse groups exhibited a Th2 phenotype with interleukin (IL)-4 and IL-5 production. TNBS colitis in normal mice treated with anti-IL-4 antibodies or in IL-4(-/-) mice was less severe than in either IFN-gamma+/+ or IFN-gamma-/- mice. Our findings now show that the Th2-type responses in TNBS colitis are associated with colonic patch enlargement and inflammation of the mucosal layer and may represent a model for ulcerative colitis.

Animals↗
PubMed2002

Bacteria-triggered CD4(+) T regulatory cells suppress Helicobacter hepaticus-induced colitis.

We have previously demonstrated that interleukin (IL)-10-deficient (IL-10 knockout [KO]) but not wild-type (WT) mice develop colitis after infection with Helicobacter hepaticus. Here, we show that infected recombination activating gene (RAG) KO mice develop intestinal inflammation after reconstitution with CD4(+) T cells from IL-10 KO animals and that the cotransfer of CD4(+) T cells from H. hepaticus-infected but not uninfected WT mice prevents this colitis. The disease-protective WT CD4(+) cells are contained within the CD45RB(low) fraction and unexpectedly were found in both the CD25(+) and the CD25(-) subpopulations of these cells, their frequency being higher in the latter. The mechanism by which CD25(+) and CD25(-) CD45RB(low) CD4(+) cells block colitis involves IL-10 and not transforming growth factor (TGF)-beta, as treatment with anti-IL-10R but not anti-TGF-beta monoclonal antibody abrogated their protective effect. In vitro, CD45RB(low) CD4(+) cells from infected WT mice were shown to produce IL-10 and suppress interferon-gamma production by IL-10 KO CD4(+) cells in an H. hepaticus antigen-specific manner. Together, our data support the concept that H. hepaticus infection results in the induction in WT mice of regulatory T cells that prevent bacteria-induced colitis. The induction of such cells in response to gut flora may be a mechanism protecting normal individuals against inflammatory bowel disease.

Adoptive Transfer↗
PubMed2005

Carbon monoxide ameliorates chronic murine colitis through a heme oxygenase 1-dependent pathway.

Heme oxygenase (HO)-1 and its metabolic product carbon monoxide (CO) play regulatory roles in acute inflammatory states. In this study, we demonstrate that CO administration is effective as a therapeutic modality in mice with established chronic colitis. CO administration ameliorates chronic intestinal inflammation in a T helper (Th)1-mediated model of murine colitis, interleukin (IL)-10-deficient (IL-10(-/-)) mice. In Th1-mediated inflammation, CO abrogates the synergistic effect of interferon (IFN)-gamma on lipopolysaccharide-induced IL-12 p40 in murine macrophages and alters IFN-gamma signaling by inhibiting a member of the IFN regulatory factor (IRF) family of transcription factors, IRF-8. A specific signaling pathway, not previously identified, is delineated that involves an obligatory role for HO-1 induction in the protection afforded by CO. Moreover, CO antagonizes the inhibitory effect of IFN-gamma on HO-1 expression in macrophages. In macrophages and in Th1-mediated colitis, pharmacologic induction of HO-1 recapitulates the immunosuppressive effects of CO. In conclusion, this study begins to elucidate potential etiologic and therapeutic implications of CO and the HO-1 pathway in chronic inflammatory bowel diseases.

Administration, Inhalation↗
PubMed2006

IL-23 plays a key role in Helicobacter hepaticus-induced T cell-dependent colitis.

Inflammatory bowel disease (IBD) is a chronic inflammatory disorder of the gastrointestinal tract that is caused in part by a dysregulated immune response to the intestinal flora. The common interleukin (IL)-12/IL-23p40 subunit is thought to be critical for the pathogenesis of IBD. We have analyzed the role of IL-12 versus IL-23 in two models of Helicobacter hepaticus-triggered T cell-dependent colitis, one involving anti-IL-10R monoclonal antibody treatment of infected T cell-sufficient hosts, and the other involving CD4+ T cell transfer into infected Rag-/- recipients. Our data demonstrate that IL-23 and not IL-12 is essential for the development of maximal intestinal disease. Although IL-23 has been implicated in the differentiation of IL-17-producing CD4+ T cells that alone are sufficient to induce autoimmune tissue reactivity, our results instead support a model in which IL-23 drives both interferon gamma and IL-17 responses that together synergize to trigger severe intestinal inflammation.

Animals↗
PubMed1999

A genomewide analysis provides evidence for novel linkages in inflammatory bowel disease in a large European cohort.

Inflammatory bowel disease (IBD) is characterized by a chronic relapsing intestinal inflammation, typically starting in early adulthood. IBD is subdivided into two subtypes, on the basis of clinical and histologic features: Crohn disease and ulcerative colitis (UC). Previous genomewide searches identified regions harboring susceptibility loci on chromosomes 1, 3, 4, 7, 12, and 16. To expand our understanding of the genetic risk profile, we performed a 9-cM genomewide search for susceptibility loci in 268 families containing 353 affected sibling pairs. Previous linkages on chromosomes 12 and 16 were replicated, and the chromosome 4 linkage was extended in this sample. New suggestive evidence for autosomal linkages was observed on chromosomes 1, 6, 10, and 22, with LOD scores of 2.08, 2.07, 2.30, and 1.52, respectively. A maximum LOD score of 1.76 was observed on the X chromosome, for UC, which is consistent with the clinical association of IBD with Ullrich-Turner syndrome. The linkage finding on chromosome 6p is of interest, given the possible contribution of human leukocyte antigen and tumor necrosis-factor genes in IBD. This genomewide linkage scan, done with a large family cohort, has confirmed three previous IBD linkages and has provided evidence for five additional regions that may harbor IBD predisposition genes.

Cohort Studies↗
PubMed1999

Linkage of inflammatory bowel disease to human chromosome 6p.

Inflammatory bowel disease (IBD) is characterized by a chronic relapsing intestinal inflammation. IBD is subdivided into Crohn disease and ulcerative colitis phenotypes. Given the immunologic dysregulation in IBD, the human-leukocyte-antigen region on chromosome 6p is of significant interest. Previous association and linkage analysis has provided conflicting evidence as to the existence of an IBD-susceptibility locus in this region. Here we report on a two-stage linkage and association analysis of both a basic population of 353 affected sibling pairs (ASPs) and an extension of this population to 428 white ASPs of northern European extraction. Twenty-eight microsatellite markers on chromosome 6 were genotyped. A peak multipoint LOD score of 4.2 was observed, at D6S461, for the IBD phenotype. A transmission/disequilibrium test (TDT) result of P=.006 was detected for D6S426 in the basic population and was confirmed in the extended cohort (P=.004; 97 vs. 56 transmissions). The subphenotypes of Crohn disease, ulcerative colitis, and mixed IBD contributed equally to this linkage, suggesting a general role for the chromosome 6 locus in IBD. Analysis of five single-nucleotide polymorphisms in the TNFA and LTA genes did not reveal evidence for association of these important candidate genes with IBD. In summary, we provide firm linkage evidence for an IBD-susceptibility locus on chromosome 6p and demonstrate that TNFA and LTA are unlikely to be susceptibility loci for IBD.

Alleles↗
PubMed2002

Human cytomegalovirus enhances chemokine production by lipopolysaccharide-stimulated lamina propria macrophages.

To elucidate the role of mucosal macrophages in intestinal human cytomegalovirus (HCMV) disease, primary lamina propria macrophages (LPM) were isolated from normal human jejunum, infected with HCMV, and studied for their cytokine responses. HCMV infection of LPM was confirmed by the presence of HCMV IE72 (UL123), pp65 (UL83), and glycoprotein B (UL55) proteins, which were detected by immunofluorescence, beginning at postinfection (pi) day 3, and were sustained through pi day 12 in 0.1%-0.5% of LPM. The late protein pp28 (UL99) was also detected up to pi day 12, consistent with productive infection. HCMV infection in LPM was characterized by quantitative competitive polymerase chain reaction, with maximum levels of HCMV DNA detected at pi day 7. HCMV infection of the LPM augmented lipopolysaccharide-inducible chemokine (interleukin [IL]-8 and macrophage inflammatory protein-1alpha) and cytokine (IL-6) production. These findings suggest that mucosal macrophages, via enhanced mediator production, play an important role in intestinal inflammation associated with HCMV infection.

AIDS-Related Opportunistic Infections↗
PubMed2003

Diagnostic accuracy of stool assays for inflammatory bacterial gastroenteritis in developed and resource-poor countries.

Because acute bacterial gastroenteritis is often inflammatory, rapid stool assays that detect intestinal inflammation might be used to distinguish between bacterial and nonbacterial gastroenteritis. We performed meta-analyses to determine the discriminatory power, in developed and in resource-poor countries, of rapid stool assays that test for lactoferrin, fecal leukocytes, fecal erythrocytes, and occult blood. In developed countries, the area under the summary receiver operating characteristic curve (AUC/SROC) was 0.89 for fecal leukocytes and 0.81 for occult blood. In resource-poor countries, the AUC/SROC was 0.79 for lactoferrin, 0.72 for fecal leukocytes, 0.63 for occult blood, and 0.61 for fecal erythrocytes. In developed countries, positive and negative likelihood ratios (LR+ and LR-, respectively) for fecal leukocytes were 4.56 and 0.32 when a threshold of >5 cells/high-power field was used, compared with 2.94 and 0.6 in resource-poor countries; for lactoferrin, LR+ was 1.34 and LR- was 0.17 in resource-poor countries when the threshold was an agglutination rating of "+" and a dilution of 1:50. In developing countries, rapid stool assays performed poorly, whereas in developed countries, tests for fecal leukocytes, lactoferrin, and occult blood were moderately useful and could identify patients who were more likely to benefit from empirical antibiotic therapy.

Developed Countries↗
PubMed2004

Enteropathogenic Escherichia coli use redundant tyrosine kinases to form actin pedestals.

Enteropathogenic Escherichia coli (EPEC) are deadly contaminants in water and food and induce protrusion of actin-rich membrane pedestals beneath themselves upon attachment to intestinal epithelia. EPEC then causes intestinal inflammation, diarrhea, and, among children, death. Here, we show that EPEC uses multiple tyrosine kinases for formation of pedestals, each of which is sufficient but not necessary. In particular, we show that Abl and Arg, members of the Abl family of tyrosine kinases, localize and are activated in pedestals. We also show that pyrido[2,3-d]pyrimidine (PD) compounds, which inhibit Abl, Arg, and related kinases, block pedestal formation. Finally, we show that Abl and Arg are sufficient for pedestal formation in the absence of other tyrosine kinase activity, but they are not necessary. Our results suggest that additional kinases that are sensitive to inhibition by PD also can suffice. Together, these results suggest that EPEC has evolved a mechanism to use any of several functionally redundant tyrosine kinases during pathogenesis, perhaps facilitating its capacity to infect different cell types. Moreover, PD compounds are being developed to treat cancers caused by dysregulated Abl. Our results raise the possibility that PD may be useful in treating EPEC infections, and because PD affects host and not bacterium, selecting resistant strains may be far less likely than with conventional antibiotics.

Actin Cytoskeleton↗
PubMed2005

Mechanism of IFN-gamma-induced endocytosis of tight junction proteins: myosin II-dependent vacuolarization of the apical plasma membrane.

Disruption of epithelial barrier by proinflammatory cytokines such as IFN-gamma represents a major pathophysiological consequence of intestinal inflammation. We have previously shown that IFN-gamma increases paracellular permeability in model T84 epithelial cells by inducing endocytosis of tight junction (TJ) proteins occludin, JAM-A, and claudin-1. The present study was designed to dissect mechanisms of IFN-gamma-induced endocytosis of epithelial TJ proteins. IFN-gamma treatment of T84 cells resulted in internalization of TJ proteins into large actin-coated vacuoles that originated from the apical plasma membrane and resembled the vacuolar apical compartment (VAC) previously observed in epithelial cells that lose cell polarity. The IFN-gamma dependent formation of VACs required ATPase activity of a myosin II motor but was not dependent on rapid turnover of F-actin. In addition, activated myosin II was observed to colocalize with VACs after IFN-gamma exposure. Pharmacological analyses revealed that formation of VACs and endocytosis of TJ proteins was mediated by Rho-associated kinase (ROCK) but not myosin light chain kinase (MLCK). Furthermore, IFN-gamma treatment resulted in activation of Rho GTPase and induced expressional up-regulation of ROCK. These results, for the first time, suggest that IFN-gamma induces endocytosis of epithelial TJ proteins via RhoA/ROCK-mediated, myosin II-dependent formation of VACs.

Actins↗
PubMed2001

Chondrocyte antigen expression, immune response and susceptibility to arthritis.

The association of HLA-B27 with certain forms of arthritis implies a role for MHC class I-restricted T cells in the arthritic process. Our aim was to study CD8(+) T cell responses towards specific antigens localized in joint tissue. Known determinants were introduced into chondrocytes of transgenic (TG) mice, under the control of the cis-regulatory sequences of the human type II collagen gene (COL2A1). Two Escherichia coli beta-galactosidase (beta-gal)-expressing lines were derived (CIIL73 and CIIL64) as well as two lines (CIINP) expressing influenza A virus nucleoprotein (NP). Expression of the antigens could be demonstrated in cartilaginous tissues. The TG lines showed variable degrees of responsiveness towards the transgene-introduced antigens; whilst 75% of CIIL73 mice had an impaired cytotoxic T lymphocyte (CTL) response towards beta-gal, the response in CIIL64 mice was essentially normal. However, both lines displayed normal proliferative and antibody responses to beta-gal. A reduced CTL response was seen to NP in the CIINP lines in approximately 65% of the animals. In spite of the persistence of T cell responses to the transgene antigens in these lines, induction of CTL responses alone has so far failed to induce clinical signs of arthritis. Interestingly, some animals expressing beta-gal were susceptible to arthritis following challenge with type II collagen alone, whilst their non-TG littermates and TG mice from other lines remained unaffected. As beta-gal is expressed by E. coli, a component of the normal gut flora, this suggests a possible role for gut-derived immune responses. We believe these lines could form the basis of a model for studying links between intestinal inflammation and arthritis.

Animals↗
PubMed1992

Transforming growth factor-beta 1 enhances IgG and IgA sheep red blood cell responses.

Antibody responses to ingested antigens can be inhibited by a mechanism known as oral tolerance which acts to prevent excessive stimulation from luminal contents. Local IgA responses can be induced in this non-responsive environment and during intestinal inflammation, mucosal IgG responses can also be increased. The purpose of this study was to compare a panel of cytokines to factors from macrophage-T cell co-culture supernatants for their ability to enhance isotype and sheep red blood cell (SRBC)-specific plaque-forming cell responses in an in vitro model of oral tolerance. IL-2, IL-4, IL-5, and IL-6, which have been implicated in IgA regulation of lipopolysaccharide-stimulated B cells, were not capable of enhancing responses in tolerized cultures; however, transforming growth factor (TGF)-beta 1 had a dose-dependent ability to enhance responses to the T cell-dependent antigen SRBCs in this system. The enhancement was only seen when antigen was present and was neutralized by specific rabbit antiserum but not normal rabbit IgG. Similar treatment of soluble factors from the macrophage-T cell co-cultures did not inhibit their ability to enhance responses suggesting at least two distinct molecular mechanisms could augment responses in tolerized cultures. This was substantiated further by showing that TGF-beta 1 was not isotype-specific. In contrast, adsorption of the macrophage-T cell co-culture supernatants against monoclonal IgA or IgG removed isotype-specific binding factors which were necessary for the enhancement of IgA and IgG respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Iron supplementation increases disease activity and vitamin E ameliorates the effect in rats with dextran sulfate sodium-induced colitis.

Inflammatory bowel disease is often associated with iron deficiency anemia and oral iron supplementation may be required. However, iron may increase oxidative stress through the Fenton reaction and thus exacerbate the disease. This study was designed to determine in rats with dextran sulfate sodium (DSS)-induced colitis whether oral iron supplementation increases intestinal inflammation and oxidative stress and whether the addition of an antioxidant, vitamin E, would reduce this detrimental effect. Four groups of rats that consumed 50 g/L DSS in drinking water were studied for 7 d and were fed: a control, nonpurified diet (iron, 270 mg, and dl-alpha-tocopherol acetate, 49 mg/kg); diet + iron (iron, 3000 mg/kg); diet + vitamin E (dl-alpha-tocopherol acetate, 2000 mg/kg) and the diet + both iron and vitamin E, each at the same concentrations as above. Body weight change, rectal bleeding, histological scores, plasma and colonic lipid peroxides (LPO), plasma 8-isoprostane, colonic glutathione peroxidase (GPx) and plasma vitamin E were measured. Iron supplementation increased disease activity as demonstrated by higher histological scores and heavier rectal bleeding. This was associated with an increase in colonic and plasma LPO and plasma 8-isoprostane as well as a decrease in colonic GPx. Vitamin E supplementation decreased colonic inflammation and rectal bleeding but did not affect oxidative stress, suggesting another mechanism for reducing inflammation. In conclusion, oral iron supplementation resulted in an increase in disease activity in this model of colitis. This detrimental effect on disease activity was reduced by vitamin E. Therefore, the addition of vitamin E to oral iron supplementation may be beneficial.

Administration, Oral↗