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PubMed2003

Surgical management of ulcerative colitis in the presence of primary sclerosing cholangitis.

INTRODUCTION: The surgical management of ulcerative colitis in the patient with primary sclerosing cholangitis is controversial. METHODS: This study was designed as a retrospective chart review of all patients with primary sclerosing cholangitis who were surgically treated for ulcerative colitis. RESULTS: Sixteen patients with primary sclerosing cholangitis and ulcerative colitis were identified. The indication for ulcerative colitis surgery was dysplasia in 7 patients (44 percent), cancer in 2 (13 percent), intractability in 4 (25 percent), and unknown in 1. Final colon pathology demonstrated cancer in three patients and dysplasia in four. Two patients had biliary cancer discovered at the time of orthotopic liver transplantation. Thirteen patients were known to have primary sclerosing cholangitis when they underwent surgery for ulcerative colitis; two patients with severe primary sclerosing cholangitis underwent simultaneous orthotopic liver transplantation/total abdominal colectomy and did well with subsequent ileal pouch reconstruction. Two patients had orthotopic liver transplantation first and then ileal pouch-anal anastomosis (1 patient) or total abdominal colectomy (1 patient) and did well. Seven patients had well-controlled primary sclerosing cholangitis on medication and underwent ileal pouch-anal anastomosis or total abdominal proctocolectomy without significant hepatic compromise. One patient with moderate primary sclerosing cholangitis underwent ileorectal anastomosis and had severe liver failure postoperatively but survived. Another patient with worsening primary sclerosing cholangitis after total abdominal colectomy has since developed persistent bleeding from peristomal varices. CONCLUSIONS: The overall cancer/premalignant lesion rate was high (50 percent in this study) in patients with primary sclerosing cholangitis and ulcerative colitis. Complications associated with the surgical management of ulcerative colitis are largely dictated by the degree of liver disease present at the time of surgery. Patients with significant primary sclerosing cholangitis that requires colectomy can undergo simultaneous orthotopic liver transplantation/total abdominal colectomy and then be candidates for subsequent ileal pouch-anal anastomosis reconstruction once liver function has improved. Patients with well-controlled primary sclerosing cholangitis can undergo ileal pouch-anal anastomosis surgery safely.

Adult↗

PubMed2006

Risk factors and indications for colectomy in ulcerative colitis patients are different according to patient's clinical background.

PURPOSE: Despite progress in medical treatment for ulcerative colitis, a considerable fraction of ulcerative colitis patients undergo colectomy. We analyzed the clinical variables of ulcerative colitis patients and determined the risk factors and indications for colectomy. METHODS: The clinical records of 981 consecutive Japanese patients with ulcerative colitis were reviewed both retrospectively and prospectively. RESULTS: Of 981 patients with ulcerative colitis, 85 patients underwent colectomy. Multivariate analysis indicated that male gender (risk ratio, 2.16; 95 percent confidence interval, 1.37-3.42), onset year during and after 2000 (risk ratio, 2.85; 95 percent confidence interval, 1.31-6.22), severe disease activity (risk ratio, 2; 95 percent confidence interval, 1.15-3.48), corticosteroid resistance (risk ratio, 7.05; 95 percent confidence interval, 4.29-11.59), and complications because of corticosteroid administration (risk ratio, 3.55; 95 percent confidence interval, 2.08-6.06) were significant risk factors for colectomy. In patients with disease duration of more than five years, only corticosteroid resistance and complications because of corticosteroid were significant risk factors for colectomy. When we stratified indications for colectomy for the 85 cases via patient disease duration, massive hemorrhage was a relatively frequent cause of colectomy in patients with a disease duration of less than five years (P = 0.091). On the other hand, colon dysplasia or cancer was a major cause for colectomy in patients with a disease duration of more than ten years (P = 0.0001). CONCLUSIONS: In ulcerative colitis patients, the risk factors and indications for colectomy were different according to the patient's clinical background. Our findings may help to predict patients with ulcerative colitis who have a high risk for colectomy.

Adrenal Cortex Hormones↗

PubMed2006

Selective COX-2 inhibition reduces leukocyte sticking and improves the microcirculation in TNBS colitis.

The role of cyclooxygenase-2 inhibitors in the course of experimental colitis is controversially discussed. The aim of this study was to evaluate leukocyte-endothelium interaction and colitis activity after applying the selective cyclooxygenase-2 inhibitor NS-398 in a rat trinitrobenzene sulfonic acid (TNBS) colitis model. The acute phase of TNBS colitis is characterized by a significant reduction of capillary blood flow, capillary density, diuresis, and weight and a significant increase in capillary permeability, leukocyte sticking, and hematocrit. Applying the selective cyclooxygenase-2 inhibitor NS-398 leads to a significant improvement of all microcirculatory parameters and clinical findings compared to the (untreated) colitis group. There are no histopathological differences between the individual colitis groups. Acute colitis is characterized by an extensive disturbance of microcirculation together with signs of systemic inflammatory response syndrome. These alterations are significantly improved by inhibiting cyclooxygenase-2. The results support the described correlation between cyclooxygenase activation and leukocyte-endothelium interaction. Moreover, they underscore the postulated relation between leukocyte-endothelium interaction and capillary blood flow.

Animals↗

PubMed2006

Increased activity and expression of gelatinases in ischemic colitis.

Ischemic colitis results from insufficient blood supply but its pathogenesis is poorly understood. The aim of this study was to determine whether the activity and expression of gelatinases (MMP-9 and MMP-2) are increased in the colonic mucosa of patients with ischemic colitis. MMP-9 and MMP-2 activity and expression were assessed in colonic mucosal specimens from 8 patients with acute ischemic colitis and in 12 controls with a normal colonoscopy. The activity and expression of MMP-9 and MMP-2 were quantified in tissue samples by zymography and western blot, respectively. Colonoscopy was repeated 12 weeks after discharge in two patients and MMP activity was assessed in the slight residual mucosal changes of ischemic colitis. In patients with ischemic colitis, a significant increase in total MMP-9 and MMP-2 activity and expression was found in ulcerated areas compared with noninvolved sites of mucosa. Following resolution of ischemic ulcers the proteolytic activity returned to baseline levels. In addition, the colonic mucosa of controls showed MMP-2 activity, whereas the MMP-9 activity was negligible or not detected. We conclude that ischemic colitis induces increased activity and expression of MMP-9 and MMP-2 in the involved colonic mucosa. These changes may contribute to tissue degradation and remodeling of the colonic mucosa in ischemic colitis.

Aged↗

PubMed1979

Necrotizing colitis in patients with cancer.

Necrotizing lesions of the colon occur in patients with malignancy. We identified 26 patients with cancer (23 with acute leukemia and three with solid tumors) who died from necrotizing colitis. Autopsies revealed three pathologic categories: pseudomembranous colitis in 69 per cent, agranulocytic colitis in 19 per cent and ischemic colitis in 12 per cent. Most died from sepsis. A comparison of characteristics was made with a control population matched for diagnosis, age, cause of death and duration of neoplasia. Nearly all patients in both groups had fever and were granulocytopenic secondary to chemotherapy. Most received antineoplastic and antimicrobial regimens during the month prior to their terminal illness. Abdominal pain and distention, stomatitis and necrotizing pharyngitis were frequently associated with colitis. Hyperbilirubinemia was a frequent late complication in those with colitis and the control group. Single and multiorganism septicemia were found more frequently in patients with colitis. As antemortem diagnosis was unusual, aggressive attempts at diagnosis are necessary to assess the true incidence of this disorder and the best therapy.

Adolescent↗

PubMed1987

Mucosal subclass distribution of immunoglobulin G-producing cells is different in ulcerative colitis and Crohn's disease of the colon.

As a marked local immunoglobulin G (IgG) response has previously been found to be the most prominent immunopathological feature of both ulcerative colitis and Crohn's disease, the subclass distribution of colonic IgG-producing immunocytes was examined. This study included tissue specimens from 10 patients with ulcerative colitis and 8 with Crohn's colitis. Paired immunofluorescence staining was performed with subclass-specific murine monoclonal antibodies combined with a rabbit antibody reagent of IgG; the proportion of cells belonging to each subclass could thereby be determined in relation to the total number of mucosal IgG immunocytes. A significantly higher median proportion of IgG1 immunocytes was found in ulcerative colitis (81.3%) than in Crohn's colitis (66.5%). Conversely, the median proportion of IgG2 immunocytes was significantly higher in Crohn's colitis (24.9%) than in ulcerative colitis (9.4%). This disparity in the local IgG subclass response might reflect dissimilar mucosal exposure to mitogenetic or antigenic stimuli or genetically determined immunoregulatory differences in the two categories of patients.

Adult↗

PubMed1990

Chemotactic peptide-induced acute colitis in rabbits.

Bacterial chemotactic peptides from the intestinal lumen could potentially induce inflammation if they reached the mucosa. We tested several peptides chemotactic for different inflammatory cells, as well as a nonchemotactic peptide, bradykinin, for their ability to induce colitis in vivo in rabbits. These peptides were also assessed for their ability to stimulate release of the eicosanoids leukotrienes B4 and C4 and prostaglandin E2 from normal rabbit colons perfused ex vivo. Intracolonic administration of n-formyl-methionyl-leucyl-phenylalanine (chemotactic for neutrophils); its methyl ester (chemotactic for monocytes), and alanyl-glycyl-seryl-glutamic acid (chemotactic for eosinophils) all produced colitis (assessed grossly and histologically) within 4 days. Bradykinin did not induce colitis although it did release prostaglandin E2. n-Formyl-methionyl-leucyl-phenylalanine methyl ester induced the greatest degree of colitis in vivo and released prostaglandin E2 and leukotrienes ex vivo. n-Formyl-methionyl-leucyl-phenylalanine and alanyl-glycyl-seryl-glutamic acid induced comparable degrees of inflammation, but alanyl-glycyl-seryl-glutamic acid produced no eicosanoid release while n-formyl-methionyl-leucyl-phenylalanine released both prostaglandin E2 and leukotriene B4 and leukotriene C4 products from normal ex vivo perfused colons. Thus alanyl-glycyl-seryl-glutamic acid produces colitis independent of proinflammatory eicosanoids while eicosanoid release could contribute to colitis produced by n-formyl-methionyl-leucyl-phenylalanine methyl ester. This experimental model of colitis may reflect one possible etiology of inflammatory bowel disease in humans, when bacterial chemotactic peptides breach mucosal defenses in susceptible individuals.

Animals↗

PubMed1990

Escherichia coli O157:H7-associated colitis. A clinical and histological study of 11 cases.

Hemorrhagic colitis is characterized by abdominal cramps, bloody diarrhea, and no or low-grade fever. Most cases are caused by the Shiga-like toxin-producing bacteria, Escherichia coli O157:H7. Nineteen colonic biopsy specimens and one resection specimen were reviewed from 11 patients with E. coli O157:H7-associated colitis to determine whether histologic features could be useful in diagnosis or in suggesting pathogenesis. All specimens showed hemorrhage and edema in the lamina propria. Specimens from nine patients were focally necrotic and showed hemorrhage and acute inflammation in the superficial mucosa with preservation of the deep crypts, similar to the pattern of injury associated with acute ischemic colitis. Specimens from five patients showed neutrophils focally infiltrating the lamina propria and crypts, resembling the pattern of injury seen in infectious colitis. One or both of these histologic patterns were observed in specimens from all but one patient. Specimens from four patients had poorly formed inflammatory pseudomembranes. It is concluded that the histologic features of E. coli O157:H7-associated colitis resemble a combination of ischemic and infectious injuries similar to those described in toxin-mediated Clostridium difficile-associated colitis. This suggests that the toxin(s) produced by these E. coliplay a role in the colonic injury. Infection with E. coli O157:H7 should be considered in the differential diagnosis of ischemic and infectious colitis.

Adult↗

PubMed1991

Colonic motility and transit in health and ulcerative colitis.

Preprandial and postprandial colonic motility and transit (scintigraphy), with respect to the splenic flexure, were studied in 10 patients with ulcerative colitis and in 9 healthy subjects. The healthy subjects had a postprandial increase in intraluminal pressure that was significantly (P less than 0.03) greater in the descending colon than in other regions of the colon. In ulcerative colitis, the pressure was decreased in all regions compared with healthy subjects, with no significant pressure gradient among different regions. In normal subjects, transit was quiescent during fasting; eating stimulated both antegrade and retrograde transit. In ulcerative colitis, transit was variable before as well as after the meal. Both healthy subjects and patients with ulcerative colitis had more rapid emptying from the splenic flexure into the sigmoid than into the transverse colon. More frequent, low-amplitude, postprandial propagating contractions occurred in ulcerative colitis (P less than 0.05) than in healthy subjects. Propagating contractions were always antegrade and caused a rapid movement of the tracer into the sigmoid. In conclusion, ulcerative colitis is characterized by (a) decreased contractility, (b) increased low-amplitude propagating contractions, and (c) variable transit. These disturbances may accentuate the diarrhea in ulcerative colitis.

Adult↗

PubMed1993

Interleukin-2 activity of colonic lamina propria mononuclear cells in a rat model of experimental colitis.

BACKGROUND: Altered interleukin 2 (IL-2) production has been implicated in the pathogenesis of inflammatory bowel diseases. METHODS: The temporal relationship between IL-2, prostaglandin E2 (PGE2) production, and mucosal injury was evaluated by isolated colonic lamina propria mononuclear cells (LPMC), using the trinitrobenzene sulfonic acid model of rat colitis. RESULTS: Spontaneous LPMC IL-2 activity was significantly increased in chronic (5 weeks) but not acute (5 days) or resolved colitis groups. IL-2 activity after concanavalin A activation was highest in the groups with resolved and chronic colitis. PGE2 production was significantly increased in LPMC cultures in acute or chronic colitis as well as the ethanol control groups but not the resolved colitis group. The addition of indomethacin to LPMC cultures decreased PGE2 levels in all groups, whereas IL-2 activity increased only for the chronic and resolved colitis groups. No correlation was found between PGE2 and IL-2 production by LPMC. CONCLUSIONS: In this experimental model, LPMC IL-2 production varied according to the severity and duration of the inflammation. Increased PGE2 production does not appear to be responsible for the IL-2 alterations in colitis.

Acute Disease↗

PubMed1992

Superior results of ileoanal pull through (IAPT) in polyposis coli vs ulcerative colitis patients.

Colectomy, mucosal proctectomy, and ileoanal pull through (IAPT) have replaced proctocolectomy as the operation of choice in most patients with the colorectal mucosal diseases ulcerative colitis and polyposis coli. This study was conducted to determine whether there is any difference in postoperative morbidity and long-term functional results when IAPT is performed for polyposis coli than when it is performed for ulcerative colitis patients. Between 1982 and 1989, 277 IAPT procedures were performed at the University of Utah Medical Center, 239 for ulcerative colitis and 38 for polyposis coli syndromes. A prospective study compared polyposis and colitis patients after IAPT with regards to age, family history, preoperative findings, operative findings, postoperative complications, and long-term complications. Functional results were compared including day and night stool frequency, incidence of nighttime incontinence, and incidence of pouchitis. The incidence of postoperative complications was lower in the polyposis group than in the colitis group, but the numbers were low enough in both diseases that significant differences were not detected. However, the incidence of pouchitis (0% vs 19%), day (4.2 vs 6.0) and night (0.4 vs 0.9) stool frequency, and nighttime incontinence (5% vs 25%) was significantly lower in the polyposis group when compared to the colitis group. We conclude that IAPT performed for polyposis conditions is associated with superior results when compared with results from patients who undergo the procedure for ulcerative colitis.

Adenomatous Polyposis Coli↗

PubMed1981

Studies of prostaglandins and sulphasalazine in ulcerative colitis.

Specific evidence is presented of the release of prostaglandins from the colon in active ulcerative colitis. An increase in the levels of bioassayed prostaglandin-like activity in the stools and colo-rectal venous plasma from patients with active ulcerative colitis is described. Radioimmunoassay confirms the presence of prostaglandin E and prostaglandin F in the stools in colitis. Increased urinary levels of prostaglandin F metabolite occur in patients with active colitis and return to normal as the disease becomes quiescent. Sulphasalazine and its faecal metabolite, 5-aminosalicylic acid, were shown by an indirect method (reduction of the tone of the isolated rat fundus strip) to inhibit prostaglandin biosynthesis in vitro. In contrast, sulphasalazine was without effect on the urinary excretion of prostaglandin F metabolite in 7 healthy subjects. In 2 patients with colitis withdrawal of sulphasalazine was associated with increasing levels of stool prostaglandin-like activity and urinary prostaglandin F metabolite excretion. Indomethacin, given to 3 patients with chronically active ulcerative colitis, unresponsive to standard medical treatment, was associated with a decreased urinary excretion of prostaglandin F metabolite but was without clinical benefit. The possible mode of action of sulphasalazine as a prostaglandin inhibitor in colitis is discussed along with the potential use of other prostaglandin inhibitors.

Adolescent↗

PubMed1995

Substance P gene expression in acute experimental colitis.

We have previously shown (Gastroenterology, 101 (1991) 1211-1219), that substance P (SP) decreases early in the colon muscle layer after induction of colitis in rabbits. Since the SP content in the colonic muscle layer was unchanged by sensory denervation with capsaicin, we assume that SP is located predominantly in intrinsic neurons of the colon, and that the decrease of SP during inflammation reflects changes in intrinsic SP content. However, damage of SP neurons by inflammation would be another likely explanation for the decrease in SP content. The aim of this study was to determine SP gene expression in intrinsic (colonic muscle layer) and extrinsic (dorsal root ganglia, DRG) neurons to prove that SP transcription is preserved during colitis as an indicator of neuronal integrity. Colitis was induced in adult white New Zealand rabbits by formalin enemas (4 ml of 0.4% formalin) followed by 0.85 ml immune complex i.v. 2 h later. The animals were sacrificed 48 h after induction of colitis, and SP content and gene expression were determined by radioimmunoassay (RIA) and Northern blot analysis, respectively. Immunoreactive SP was reduced by 40% in the colon muscle layer and by 60% in the dorsal root ganglia (L4-S4) in the animals with colitis compared to controls without colitis. In contrast to the protein data, SP gene expression was not significantly altered in the colon muscle layer and the dorsal root ganglia 48 h after induction of inflammation compared to the control tissue. The preserved SP gene expression suggests that the intrinsic and extrinsic SP neurons are viable in this inflammatory model. The decreases of immunoreactive SP in the colonic extracts and the DRG after induction of colitis suggest that SP is released from extrinsic and intrinsic neurons during inflammation.

Acute Disease↗

PubMed2005

Predisposition to colorectal cancer in rats with resolved colitis: role of cyclooxygenase-2-derived prostaglandin d2.

Colitis markedly increases the risk of developing colon cancer, but the underlying mechanisms are not fully understood. In a rat model of colitis, alterations in epithelial secretion, proliferation, and barrier function persist long after healing has occurred. In the present study, we examined whether rats that have recovered from a bout of colitis are more susceptible to preneoplastic lesions and whether this susceptibility is mediated by cyclooxygenase (COX)-2-derived prostaglandin (PG) D2. Colitis was induced by intracolonic administration of trinitrobenzenesulfonic acid. Six weeks later, weekly treatment with the carcinogen azoxymethane was initiated. Postcolitis rats exhibited significantly more aberrant crypt foci after azoxymethane treatment than controls. The postcolitis rats also exhibited markedly increased colonic PGD2 synthesis and elevated COX-2, H-PGD synthase, and beta-catenin expression. Treatment for 1 week with a selective COX-2 inhibitor or with a selective PGD2 receptor (DP1) antagonist significantly reduced susceptibility of postcolitis rats to aberrant crypt foci development, beta-catenin expression, and mucosal thickness. The results from this animal model suggest that prolonged elevation of COX-2-derived PGD2 synthesis after resolution of colitis may contribute significantly to colitis-associated increases in colon cancer incidence. PGD2 may therefore represent a rational target for therapies directed at reducing the incidence of colitis-associated colorectal cancer.

Animals↗

PubMed2002

Anorexia in a rat model of colitis: interaction of interleukin-1 and hypothalamic serotonin.

BACKGROUND AND AIMS: Anorexia induced by experimental colitis in rats is mediated, in part, by increased release of serotonin (5-HT) from the hypothalamic paraventricular nucleus (PVN). In this model, anorexia is attenuated by treatment with an interleukin-1 (IL)-1 receptor antagonist (ra). However, a functional link between central IL-1 receptors and 5-HT release remains unproven. We have tested the hypothesis that anorexia associated with experimental colitis is mediated by IL-1 induced release of 5-HT. METHODS: In vivo 5-HT release in the PVN was measured in rats with 2,4,6-trinitrobenzenesulphonic acid (TNBS)-induced colitis, treated with intracerebroventricular infusion of IL-1ra or vehicle treated controls. The effect of inhibition of tumour necrosis factor-alpha on food intake and PVN 5-HT release in TNBS-colitis was also tested. RESULTS: In rats with TNBS-induced colitis, intracerebroventricular infusion of IL-1ra resulted in a 18-fold reduction in PVN 5-HT release compared to vehicle-treated controls. This was associated with a significant increase in food intake in IL-1ra treated rats. In contrast intracerebroventricular administration of anti-tumour necrosis factor antibodies had no effect on either PVN 5-HT release or food intake in rats with TNBS-induced colitis. CONCLUSIONS: In animals with TNBS-colitis, anorexia is mediated, in part, by the stimulatory effect of IL-1 on medial hypothalamic 5-HT.

Animals↗

PubMed2001

Acute effects of the cys-leukotriene-1 receptor antagonist, montelukast, on experimental colitis in rats.

Cysteinyl leukotrienes play a part in inflammatory reactions such as inflammatory bowel diseases. The aim of the present study was to evaluate the acute effects of a cys-leukotriene-1 receptor antagonist, montelukast, on trinitrobenzene sulphonic acid (TNBS)-induced colitis in rats. Montelukast (5, 10 or 20 mg kg(-1) day(-1)), a 5-lipoxygenase inhibitor, zileuton (50 or 100 mg kg(-1) day(-1), a positive control), or the vehicle was administered intracolonically to the rats twice daily throughout the study, starting 12 h before the induction of colitis with TNBS. The severity of colitis (macroscopic and histological assessment, as well as myeloperoxidase activity), the protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2, and eicosanoid production in colonic tissue incubation were assessed 24 and 72 h after colitis induction. Montelukast increased prostaglandin E(2) production at 24 h and tended to reduce the cyclooxygenase-2 protein expression at 72 h, but did not influence the severity of colitis. Zileuton failed to decrease the inflammatory reaction in spite of reduced leukotriene B(4) production at 72 h. The results suggest that drugs that block cysteinyl leukotriene receptors have limited potential to ameliorate acute TNBS-induced colitis, but that they exert some beneficial effects which make them capable of modulating the course of colitis.

Acetates↗

PubMed2003

Bacteroides vulgatus protects against Escherichia coli-induced colitis in gnotobiotic interleukin-2-deficient mice.

BACKGROUND & AIMS: The microflora plays a crucial role in inflammatory bowel diseases (IBDs). Specific pathogen-free (SPF), but not germ-free, interleukin (IL)-2-deficient (IL-2-/-) mice develop colitis. The colitogenicity of commensal bacteria was determined. METHODS: Gnotobiotic IL-2-/- and IL-2+/+ mice were colonized with Escherichia coli mpk, Bacteroides vulgatus mpk, or both bacterial strains, or with E. coli strain Nissle 1917. DNA arrays were used to characterize E. coli mpk. Colitis was analyzed by histology and real-time reverse-transcription polymerase chain reaction (RT-PCR) for interferon (IFN)-gamma, tumor necrosis factor (TNF)-alpha, IL-10, and CD14 messenger RNA (mRNA) expression. Bacterial numbers in feces and bacterial localization in the colon was determined by culture and fluorescence in situ hybridization (FISH). RESULTS: IL-2-/- but not IL-2+/+ mice monocolonized with E. coli mpk developed colitis, whereas mono-association with B. vulgatus mpk, or E. coli Nissle, or co-colonization with E. coli mpk and B. vulgatus mpk, did not induce colitis. DNA array experiments and cellular studies revealed that E. coli mpk is a nonpathogenic strain. FISH and culture methods revealed that the anticolitogenic effect of B. vulgatus mpk on E. coli mpk cannot be explained by a significant reduction in numbers of E. coli in the colon. E. coli mpk-induced colitis was associated with increased IFN-gamma, TNF-alpha, CD14, and IL-10 mRNA expression in the colon. CONCLUSIONS: In IL-2-/- mice, B. vulgatus mpk protects against E. coli mpk-triggered colitis by an unknown mechanism. E. coli Nissle does not induce colitis. Various bacterial species common to the microflora differ in their ability to trigger IBD.

Animals↗

PubMed2003

Dietary glycine prevents chemical-induced experimental colitis in the rat.

BACKGROUND & AIMS: In this study, the effect of dietary glycine on experimental colitis induced by 2,4,6-trinitrobenzene sulphonic acid (TNBS) and dextran sulfate sodium (DSS) in the rat was evaluated. METHODS: Male Wistar rats were fed a diet containing 5% glycine or casein as controls starting 3 days before experiments, and were given a single intracolonic injection of TNBS (50 mg/rat, dissolved in 50% ethanol). Similarly, some rats were given 3% DSS orally in drinking water for 5 days to induce colitis as a second model. The severity of colitis was evaluated pathologically, and tissue myeloperoxidase (MPO) activity was measured. Further, mRNA and protein levels for interleukin (IL)-1beta, tumor necrosis factor (TNF)-alpha, cytokine-induced neutrophil chemoattractant (CINC), and macrophage inflammatory protein (MIP)-2 were detected by reverse-transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA), respectively. RESULTS: A diet containing glycine ameliorated diarrhea and body weight loss caused by TNBS, and improved both macroscopic and histologic scores of colitis significantly. TNBS-induced increases in MPO activities in the colonic tissue were blunted significantly in glycine-fed animals. Further, dietary glycine largely prevented increases in IL-1beta and TNF-alpha in the colon 2 days after TNBS, and TNBS induction of CINC and MIP-2 in the colonic tissue also was abrogated by glycine. Importantly, the protective effect of glycine was significant even when TNBS colitis was once established. Moreover, dietary glycine also was preventive in a second, DSS-induced colitis model. CONCLUSIONS: Dietary glycine prevents chemical-induced colitis by inhibiting induction of inflammatory cytokines and chemokines. It is postulated that glycine may be useful for the treatment of inflammatory bowel diseases as an immunomodulating nutrient.

Animals↗