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PubMed2006

Involvement of lymphocytes in dextran sulfate sodium-induced experimental colitis.

AIM: To investigate the roles of lymphocytes in the development of dextran sulfate sodium-induced colitis. METHODS: Using various doses of dextran sulfate sodium (DSS), we induced colitis in wild-type B6 control and Rag-1 knockout (H-2b haplotype) mice, and evaluated the colitis in terms of symptomatic and histologic parameters, such as weight loss, survival, severity of diarrhea, shortage of colon length and histological changes. Symptomatic parameters were checked daily and histological changes were scored. RESULTS: Although development of colitis in Rag-1 knockout mice treated with high dose (5%) of DSS was comparable to that in B6 control mice, colitis progression was much more tolerable in Rag-1 knockout mice compared to than in B6 mice treated with low dose (1.5%) DSS. Symptomatic parameters as well as histopathologic changes were improved in Rag-1 knockout mice. CONCLUSION: These results indicate that the presence of lymphocytes contributes to colitis progression at low dose of DSS stimulation. Lymphocytes may play roles as an aggravating factor in DSS-induced colitis.

Animals↗
PubMed2006

Microheterogeneity of acute phase proteins in patients with ulcerative colitis.

AIM: To estimate the serum alpha1-antichymotrypsin (ACT), alpha1-acid glycoprotein (AGP) and transferrin (Tf) concentrations and to evaluate the microheterogeneity of these acute phase proteins in patients with ulcerative colitis. METHODS: Twenty-seven patients with ulcerative colitis (UC) and 17 healthy control subjects were studied. The patients were categorised as severe (n = 9), moderate (n = 10) and mild groups (n = 8) using Truelove and Witts' classification of ulcerative colitis. Microheterogeneity of ACT, AGP and Tf was analysed by crossed immunoaffinity electrophoresis (CIAE) with concanavalin A. In all serum samples standard electrophoresis of serum proteins was performed, iron (Fe) concentration, total iron binding capacity (TIBC) and C-reactive protein (CRP) were also measured. RESULTS: Our patients suffering from ulcerative colitis had significantly higher serum ACT and AGP concentrations and lower serum transferrin concentration in comparison to healthy subjects. Changes in concentrations of acute phase proteins were dependent on the activity of the inflammatory process. The glycosylation patterns of transferrin were related to the inflammation status. We also observed the correlation between ACT and AGP concentrations, patterns of transferrin glycosylation and changes in standard protein electrophoresis or blood cell count. CONCLUSION: The glycosylation patterns of transferrin obtained from patients suffering from ulcerative colitis are highly branched and sialylated compared with those obtained from healthy subjects. In contrast, the glycosylation patterns of transferrin do not differ according to the activity index of ulcerative colitis. The microheterogeneity patterns of AGP and ACT are similar in ulcerative colitis patients and healthy subjects.

Acute-Phase Proteins↗
PubMed2006

Defensin expression in chronic pouchitis in patients with ulcerative colitis or familial adenomatous polyposis coli.

AIM: Pouchitis develops in ileoanal pouches in up to 50% of patients with ulcerative colitis during the first 10 years after pouch surgery while being rare in patients after proctocolectomy for familial adenomatous polyposis coli (FAP) syndrome. Defensins are major components of the innate immune system and play a significant role in gastrointestinal microbial homeostasis. Pouch defensin and cytokine expression were correlated with states of pouch inflammation to study their role in pouchitis. METHODS: Patients with ulcerative colitis and FAP syndrome were stratified into groups with pouches after surgery, pouches without or with pouchitis. Biopsies from terminal ileum from a healthy intestine or from normal terminal ileum of patients with ulcerative colitis served as controls. mRNA from pouches and controls was analysed for defensin and cytokine expression. RESULTS: Expression of defensins was increased in all pouches immediately after surgery, compared to ileum of controls. Initially, pouches in ulcerative colitis revealed higher defensin expression than FAP pouches. Defensin expression declined in both patient groups and increased again slightly in pouchitis in patients with ulcerative colitis. FAP pouches without pouchitis had strong expression of beta-defensin hBD-1, while all other defensins remained at low levels. Cytokine expression in ulcerative colitis pouches was high, while FAP pouches showed moderately elevated cytokines only after surgery. CONCLUSION: Development of pouchitis correlates with decreased defensin expression in ulcerative colitis in addition to high expression of cytokines. The low incidence of pouchitis in FAP pouches correlates with increased expression of hBD-1 beta-defensin in association with low cytokine levels.

Adenomatous Polyposis Coli↗
PubMed2003

Primary biliary cirrhosis and ulcerative colitis: a case report and review of literature.

AIM: To summarize the characteristics of patients suffered from primary biliary cirrhosis associated with ulcerative colitis. METHODS: To report a new case and review the literature. RESULTS: There were 18 cases (including our case) of primary biliary cirrhosis complicated with ulcerative colitis reported in the literature. Compared with classical primary biliary cirrhosis, the patients were more often males and younger similar. The bowel lesions were usually mild with proctitis predominated. While ulcerative colitis was diagnosed before primary biliary cirrhosis in 13 cases, the presentation of primary biliary cirrhosis was earlier than that of ulcerative colitis in our new case reported here. The prevalence of primary biliary cirrhosis among patients of ulcerative colitis was almost 30 times higher than in general population. CONCLUSION: Association of primary biliary cirrhosis with ulcerative colitis is rare. It should be considered in the differential diagnosis of hepatobiliary disease in patients with ulcerative colitis, and vice versa.

Adult↗
PubMed2001

Oral administration of recombinant cholera toxin subunit B inhibits IL-12-mediated murine experimental (trinitrobenzene sulfonic acid) colitis.

Trinitrobenzene sulfonic acid (TNBS)-induced colitis is an IL-12-driven, Th1 T cell-mediated colitis that resembles human Crohn's disease. In the present study, we showed initially that the oral administration of recombinant subunit B of cholera toxin (rCT-B) at the time of TNBS-induced colitis by intrarectal TNBS instillation inhibits the development of colitis or, at later time when TNBS-induced colitis is well established, brings about resolution of the colitis. Dose-response studies showed that a majority of mice (68%) treated with rCT-B at a dose of 100 microg (times four daily doses) exhibited complete inhibition of the development of colitis, whereas a minority (30%) treated with rCT-B at a dose of 10 microg (times four daily doses) exhibited complete inhibition; in both cases, however, the remaining mice exhibited some reduction in the severity of inflammation. In further studies, we showed that rCT-B administration is accompanied by prevention/reversal of increased IFN-gamma secretion (the hallmark of a Th1 response) without at the same time causing an increase in IL-4 secretion. This decreased IFN-gamma secretion was not associated with the up-regulation of the secretion of counterregulatory cytokines (IL-10 or TGF-beta), but was associated with a marked inhibition of IL-12 secretion, i.e., the secretion of the cytokine driving the Th1 response. Finally, we showed that rCT-B administration results in increased apoptosis of lamina propria cells, an effect previously shown to be indicative of IL-12 deprivation. From these studies, rCT-B emerges as a powerful inhibitor of Th1 T cell-driven inflammation that can conceivably be applied to the treatment of Crohn's disease.

Administration, Oral↗
PubMed2004

Expression of dual TCR on DO11.10 T cells allows for ovalbumin-induced oral tolerance to prevent T cell-mediated colitis directed against unrelated enteric bacterial antigens.

The triggering Ag for inflammatory bowel disease and animal models of colitis is not known, but may include gut flora. Feeding OVA to DO11.10 mice with OVA-specific transgenic (Tg) TCR generates Ag-specific immunoregulatory CD4(+) T cells (Treg) cells. We examined the ability of oral Ag-induced Treg cells to suppress T cell-mediated colitis in mice. SCID-bg mice given DO11.10 CD4(+)CD45RB(high) T cells developed colitis, and cotransferring DO11.10 CD45RB(low)CD4(+) T cells prevented CD4(+)CD45RB(high) T cell-induced colitis in the absence of OVA. The induction and prevention of disease by DO11.10 CD4(+) T cell subsets were associated with an increase in endogenous TCRalpha chain expression on Tg T cells. Feeding OVA to SCID-bg mice reconstituted with DO11.10 CD4(+)CD45RB(high) attenuated the colitis in association with increased TGF-beta and IL-10 secretion, and decreased proliferative responses to both OVA and cecal bacteria Ag. OVA feeding also attenuated colitis in SCID-bg mice reconstituted with a mix of BALB/c and DO11.10 CD45RB(high) T cells, suggesting that OVA-induced Treg cells suppressed BALB/c effector cells. The expression of endogenous non-Tg TCR allowed for DO11.10-derived T cells to respond to enteric flora Ag. Furthermore, feeding OVA-induced Treg cells prevented colitis by inducing tolerance in both OVA-reactive and non-OVA-reactive T cells and by inducing Ag-nonspecific Treg cells. Such a mechanism might allow for Ag-nonspecific modulation of intestinal inflammation in inflammatory bowel disease.

Administration, Oral↗
PubMed2004

Protective role of arginase in a mouse model of colitis.

Arginase is the endogenous inhibitor of inducible NO synthase (iNOS), because both enzymes use the same substrate, l-arginine (Arg). Importantly, arginase synthesizes ornithine, which is metabolized by the enzyme ornithine decarboxylase (ODC) to produce polyamines. We investigated the role of these enzymes in the Citrobacter rodentium model of colitis. Arginase I, iNOS, and ODC were induced in the colon during the infection, while arginase II was not up-regulated. l-Arg supplementation of wild-type mice or iNOS deletion significantly improved colitis, and l-Arg treatment of iNOS(-/-) mice led to an additive improvement. There was a significant induction of IFN-gamma, IL-1, and TNF-alpha mRNA expression in colitis tissues that was markedly attenuated with l-Arg treatment or iNOS deletion. Treatment with the arginase inhibitor S-(2-boronoethyl)-l-cysteine worsened colitis in both wild-type and iNOS(-/-) mice. Polyamine levels were increased in colitis tissues, and were further increased by l-Arg. In addition, in vivo inhibition of ODC with alpha-difluoromethylornithine also exacerbated the colitis. Taken together, these data indicate that arginase is protective in C. rodentium colitis by enhancing the generation of polyamines in addition to competitive inhibition of iNOS. Modulation of the balance of iNOS and arginase, and of the arginase-ODC metabolic pathway may represent a new strategy for regulating intestinal inflammation.

Animals↗
PubMed1999

Colorectal cancer complicating ulcerative colitis: an institutional series.

Ulcerative colitis predisposes to colorectal cancer: the risk increases along with disease duration and extension. Also some subsets of patients are at increased risk, namely patients with early onset of colitis, and patients with primary sclerosing cholangitis. Cancer complicating ulcerative colitis affects evenly all the colon, and is not located more frequently in the rectum and in the sigmoid colon, as well as the sporadic counterpart. Multiple cancers and cancers associated with high grade dysplasia are not infrequent in ulcerative colitis; for this reason, and for controlling the colitis, the treatment of choice is total colectomy, with or without colostomy. The prognosis of cancer complicating ulcerative colitis is similar to the sporadic counterpart. The Authors present a colon cancers series as a complication of colitis occurred at Regina Elena Cancer Institute of Rome, Italy, over the period 1975-1998.

Adult↗
PubMed1999

[Unusual form of ulcerative colitis].

Segmental colitis which showed the similar findings of ulcerative colitis and right-sided colitis with back-wash ileitis has been considered as the unusual form of ulcerative colitis. Today, we have few opportunities to come across those cases, because modern diagnosis of colon disease could make differential diagnosis easily with the sense of broad spectrum of IBD. We presented three cases of segmental colitis and one case of so-called indeterminate colitis associated of carcinoma in the cecum and discussed the clinical significance for diagnosis and finding the step of studying the etiology of IBD. Especially, in the third case, thirteen years old man was showing the sign of early stage of Crohn disease with non-caseating granuloma in the biopsy specimen at first, the findings of the segmental ulcerative colitis with crypt abscess were seen after six months in the second examination. To observe the detail changes of the mucosal lesion in this kind of cases will present the new idea for studying the etiology of IBD.

Adolescent↗
PubMed2000

Medical and surgical management of severe colitis.

The management of severe ulcerative colitis and Crohn's colitis remains a challenge, despite significant advances in medical and surgical therapy. Optimal management of the patient with severe colitis requires close collaboration between the gastroenterologist and surgeon. All patients with severe colitis should be hospitalized and treated with intravenous corticosteroids. If significant improvement does not occur within 7 to 10 days, then intravenous cyclosporine therapy or surgery is appropriate. Newer medical therapies, including heparin, tacrolimus, and other immunomodulatory agents, show promise for the treatment of severe colitis. When surgery is necessary, a total abdominal colectomy with ileostomy is the appropriate surgical intervention in most cases. In patients presenting with fulminant colitis, toxic megacolon, or perforation, earlier surgical intervention is indicated. The evaluation of and approach to the medical and surgical management of severe colitis will be reviewed.

Adrenal Cortex Hormones↗
PubMed1999

Spectrum of acute self-limiting colitis: role of the clinician and pathologist.

Acute self-limited colitis encompasses several diagnostic possibilities such as infectious colitis, post-antibiotic colitis, drug-induced colitis and should be differentiated from acute forms of inflammatory bowel disease. Diverticular disease in the elderly patient with colonic ischaemia may also give symptoms of acute bloody mucoid rectal discharge and should be recognised, although the clinical picture is usually completely different. Recognition of the causative agent--if possible--is particularly important in the patient with a foudroyant colitis (e.g. toxic megacolon), when the clinician has to decide, whether antibiotics or corticosteroids should be given or even a resection should be performed. A short history usually indicates towards infection, but a long-standing history of inflammatory bowel disease may be complicated by a superinfection. Faecal cultures, endoscopy with colonic biopsy should be performed and results be discussed. New techniques for the assessment and follow up of difficult cases are: white cell scintigraphy, computerized tomography scanning and magnetic resonance imaging scanning. Acute self-limited colitis can usually be classified properly and treated accordingly. This review discusses the role to be played by the clinician, microbiologist and pathologist and is illustrated by several clinical examples, in which patients presented with unusual forms of acute self-limited colitis.

Acute Disease↗
PubMedDate not supplied

Peptidergic nerves in the colon of patients with ulcerative colitis.

BACKGROUND/AIMS: The cause of impaired motility, such as diarrhea and toxic megacolon, in patients with ulcerative colitis is unknown. Neuropeptides have recently been shown to be a neurotransmitter in the non-adrenergic non-cholinergic inhibitory and excitatory nerves in the human gut. To clarify the physiological significance of vasoactive intestinal polypeptide, substance P and neurotensin in the colon of patients with ulcerative colitis, we investigated the enteric nerve responses on lesional and normal bowel segments derived from patients with ulcerative colitis and patients who underwent colon resection for colonic cancers. METHODOLOGY: Twenty-four specimens were obtained from the lesional colon of 6 patients with ulcerative colitis (4 male, 2 female; ages 14-51 years, mean: 40.3 years). The patients with ulcerative colitis had chronic disease (4 with moderate disease, 2 with severe disease). Seventy-two specimens were obtained from the normal colon of 10 patients with colonic cancer (8 men and 2 women; ages 40-56 years, mean: 51.2 years). A mechanographic technique was used to evaluate in vitro muscle responses to these peptides of adrenergic and cholinergic nerves before and after treatment with various autonomic nerve blockers. RESULTS: (1) Peptidergic nerves such as vasoactive intestinal polypeptide, substance P, and neurotensin nerves were found to act on both normal colon and ulcerative colitis colon; (2) the colon with ulcerative colitis was more strongly innervated by vasoactive intestinal polypeptide nerves than the normal colon; (3) Substance P and neurotensin nerves act more weakly in the UC colon that the normal colon. CONCLUSIONS: These findings suggest that peptidergic nerves play an important role in the impaired motility observed in patients with UC.

Adolescent↗
PubMed2000

Dose-dependent effects of recombinant human interleukin-11 on contractile properties in rabbit 2,4,6-trinitrobenzene sulfonic acid colitis.

We studied the effect of recombinant human interleukin-11 (rhIL-11), a cytokine with protective effects against injury to the intestinal mucosa, on inflammatory changes in the muscle layers of the gut, in rabbits with colitis. A single dose of rhIL-11 (4, 40, or 720 microg/kg) was given 1 h before colitis was induced with 135 mg/kg 2, 4,6-trinitrobenzene sulfonic acid (TNBS), followed by a continuous s. c. administration of 4, 40, or 720 microg/kg. day rhIL-11 or saline for 5 days. Colitis affected mucosal architecture, general mechanical properties (passive tension increased with 12.3 g/mm(2), optimal stretch decreased with 26%), and collagen content (decreased from 366 +/- 25 to 237 +/- 13 microg/mg of protein). Changes in passive tension and collagen content were normalized by the highest and lowest dose of rhIL-11, respectively, but neither dose could normalize the optimal stretch. Colitis also decreased maximal contractile tension in response to acetylcholine (ACh), motilin, substance P (SP), K(+), and prostaglandin E(2) but this was normalized with 40 microg/kg. day (motilin, SP) and 720 microg/kg. day (ACh, K(+)) rhIL-11 but not for prostaglandin E(2). For motilin and SP, receptor density was decreased in colitis and normalized in treated rabbits. Colitis also increased the contractile potency toward ACh, an effect already reversed by rhIL-11, 4 microg/kg. day. In conclusion, rhIL-11 partially normalizes disturbed tension generation in experimental colitis. The use of this cytokine in the treatment of irritable bowel disease may contribute to the restoration of motor dysfunction.

Acetylcholine↗
PubMed2001

Suppression of acute experimental colitis by a highly selective inducible nitric-oxide synthase inhibitor, N-[3-(aminomethyl)benzyl]acetamidine.

High concentrations of nitric oxide (NO) produced by the inducible nitric-oxide synthase (iNOS) are associated with ulcerative inflammation and disease activity in colitis. Therefore, inhibition of iNOS serves as a novel experimental approach to treat gut inflammation. The aim of the present study was to investigate the effects of a novel highly selective iNOS inhibitor, N-[3-(aminomethyl)benzyl]acetamidine (1400W), as compared with a nonselective NOS inhibitor, N(G)-nitro-L-arginine-methyl-ester (L-NAME), in 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced acute colitis in the rat. Increased expression of iNOS protein and mRNA was found in acute TNBS-induced colitis along with neutrophil infiltration, inflammatory edema, and tissue damage. In a 24-h model of acute colitis, subcutaneous injections of 1400W (5 or 10 mg/kg t.i.d.) produced a 56 and 95% reduction in inflammatory edema formation, a 68 and 63% reduction in neutrophil infiltration (measured as myeloperoxidase activity), and a 19 and 26% decrease in the size of mucosal lesions as compared with vehicle treatment. Administration of L-NAME (35 mg/kg) failed to produce any significant beneficial effects as compared with vehicle treatment in this experimental model of acute colitis. Treatment with 1400W, a highly selective inhibitor of iNOS, reduced formation of edema, neutrophil infiltration, and macroscopic inflammatory damage in experimentally induced acute colitis in the rat. In contrast, nonselective nitric-oxide synthase inhibition with L-NAME provided no benefit. These results support the idea that selective iNOS inhibitors have a promise in the treatment of colitis.

Amidines↗
PubMed1998

[The effect of interleukin-1 beta interleukin-8 in the pathogenesis of experimental colitis and evaluation of interleukin-1 receptor antagonist therapy].

OBJECTIVE: To study the effect of interleukin-1 beta and interleukin-8 in the pathogenesis of colitis and evaluate the therapeutic effect of interleukin-1 receptor antagonist(IL-1ra). METHODS: A rat model of chronic experimental colitis was induced by administration of trinitrobenzenesulfonic acid (TNBS, 30 mg) in 50% ethanol 0.25 ml. IL-1ra was then administered intravenously with a dosage of 7 mg/kg at different times. Hydrocortisone (3 mg) i.v. administration was served as control. Tissue expression of IL-1 beta mRNA and IL-8 mRNA was then studied by in situ hybridization before and after IL-1ra administration. Histological examination and tissue myeloperoxidase (MPO) and superoxide dismutase (SOD) activities detection were also made to assess the severity of colitis. RESULTS: An acute inflammation with ulcers, neutrophil infiltration and crypt abscess developed that evolved into a chronic inflammation with abundant fibrous connective tissue hypertrophy at 21 days. And it then recurs only after 10 mg TNBS administration. Activities of MPO and SOD correlated with severity of inflammation. Expression of IL-1 beta mRNA was detected in macrophages in lamina propria and submucosa during the whole period of inflammation. It could be also present in epithelial cells in the 3rd day of colitis. While IL-8 mRNA expression appeared at the 3rd day, and disappeared at 21th day when colitis turned into chronic. After IL-1ra administration, the expression of these two interleukins could not be detected, accompanied with alleviation of histological manifestation, decrease of MPO activity and elevation of SOD activity. CONCLUSIONS: IL-1 beta and IL-8 were involved in the pathogenesis of colitis. IL-1ra has preventive and therapeutic effect to colitis.

Animals↗
PubMed2002

Prebiotic treatment of experimental colitis with germinated barley foodstuff: a comparison with probiotic or antibiotic treatment.

There is increasing evidence that intestinal microflora play an important role in the pathogenesis of ulcerative colitis. Therefore, modification of the microflora by prebiotics, probiotics, and antibiotics may be a rational approach for controlling intestinal inflammation. Germinated barley food-stuff (GBF) is an insoluble mixture of glutamine-rich protein and hemicellulose-rich dietary fiber. GBF is utilized efficiently by Bifidobacterium, Lactobacillus, and Eubacterium and converted by them into lactate, acetate, and butyrate. These bacterial organic acids preserve a favorable intestinal condition. We have previously shown that GBF has attenuated intestinal inflammation in patients with ulcerative colitis and experimental colitis models through prebiotic actions. The aim of this study was to compare the effect of GBF with that of probiotics and antibiotics in an experimental colitis model. Colitis was induced by feeding male SD rats with a diet containing 3.0-3.5% dextran sodium sulfate (DSS). The therapeutic effect of oral administration of a prebiotic (GBF), probiotics (mixture of Lactobacillus and Clostridium butyricum), antibiotics (vancomycin, metronidazole), and the vehicle was determined by assessing clinical and pathological scores on day 6 after initiation of colitis. Butyrate concentrations in the cecal content were also determined. GBF treatment significantly reduced colonic inflammation as assessed by clinical scores with an increase in cecal butyrate levels. Probiotic treatment with a mixture of Lactobacillus and Clostridium butyricum did not show such an effect. Both antibiotic treatments significantly attenuated clinical and pathological scores. However, in contrast to GBF, this treatment led to a significant decrease in cecal butyrate levels. These data suggest that modification of the intestinal microflora by prebiotics, including GBF, may serve as a useful adjunct in the treatment of ulcerative colitis as well as antibiotic treatment.

Animal Feed↗
PubMed2002

[Microscopic colitis].

Microscopic colitis is an umbrella term for a newly described group of colitides, belonging to the inflammatory bowel diseases, which are only diagnosable by microscopic evaluation of a macroscopically normal colon mucosa. Collagenous colitis and lymphocytic colitis are the most common of these colitides. Microscopic colitis is characterised clinically by chronic non-bloody watery diarrhoea. Crampy abdominal pain, nocturnal diarrhoea, urgency, and initial weight loss are usual. Concomitant diseases of autoimmune origin and arthralgia are commonly seen. Treatment of microscopic colitis follows the guidelines for treatment of other inflammatory bowel diseases, but a substantial part of the patients with microscopic colitis enter spontaneous remission after some years. A minor part, however, have very troublesome symptoms and are almost refractory to treatment. Microscopic colitis has apparently no malignant potential.

Chronic Disease↗
PubMed1992

Granulocyte infiltration in experimental colitis in the rat is interleukin-1 dependent and leukotriene independent.

Intracolonic administration of trinitrobenzene sulfonic acid in ethanol results in the development of colitis in the rat. Previous studies have demonstrated that the severity of this colitis can be markedly reduced by repeated treatment with inhibitors of leukotriene synthesis, although such treatment does not appear to affect the initial migration of granulocytes into the colon. The present study evaluated the contribution of leukotrienes and interleukin-1 to the recruitment of granulocytes into the colon during the first 12 h after induction of colitis. Rats were treated with a leukotriene synthesis inhibitor (PF-5901), a leukotriene B4 receptor antagonist (SC-41930), an IL-1 receptor antagonist or a corticosteroid (prednisolone) prior to induction of colitis. Granulocyte infiltration was assessed by measurement of colonic myeloperoxidase activity and severity of colonic damage was blindly scored. Despite significant inhibition of leukotriene synthesis, PF-5901 did not affect colonic myeloperoxidase activity or the severity of colonic injury at any time point. Similarly, SC-41930 was without significant effect. However, both the interleukin-1 receptor antagonist and prednisolone significantly reduced colonic myeloperoxidase activity (by approximately 50%) and severity of colonic damage at 6 h after induction of colitis, without significantly affecting colonic leukotriene synthesis. These beneficial effects were no longer apparent at 12 h after induction of colitis. This study demonstrates that the infiltration of granulocytes into the colon during the acute phase of colitis in the rat occurs independent of leukotriene synthesis and appears to be at least in part attributable to interleukin-1.

Analysis of Variance↗