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PubMed1991

Defect in colonic smooth muscle contraction in patients with ulcerative colitis.

Patients with ulcerative colitis have decreased postprandial colonic contractions. The purpose of this study was to determine whether the smooth muscle from patients with ulcerative colitis responds abnormally in vitro to different stimuli. Circular colonic smooth muscle strips from patients with ulcerative colitis, acute diverticular disease, or adenocarcinoma were stretched to the optimal length and stimulated with electrical field stimulation (EFS), bethanechol, or increased concentrations of extracellular K+. The EFS-stimulated on-contraction was similar in each group, but the off-contraction was decreased in patients with colitis compared with patients with cancer (P less than 0.02) or diverticular disease (P less than 0.01). Bethanechol stimulated a dose-dependent colonic contraction, which was less in the strips from patients with colitis compared with cancer (P less than 0.02) or diverticular disease (P less than 0.05). The response to increased extracellular K+ was less in muscle from patients with colitis (P less than 0.01) than in the other tissues. Muscle from diverticular disease developed greater stress to K+ stimulation than did muscle from cancer (P less than 0.05). These studies suggest that there is a decrease in the force of muscle contraction in colonic muscle obtained from patients with colitis compared with normal muscle resected from patients with cancer or with muscle associated with diverticular disease of the colon. The similar relatively low amplitude of the on-contraction in each group suggests the physiological release of an inhibitory neurotransmitter.

Adenocarcinoma↗
PubMedDate not supplied

Failure of added dietary gluten to induce small intestinal histopathological changes in patients with watery diarrhea and lymphocytic colitis.

Lymphocytic colitis is a form of microscopic colitis usually characterized by watery diarrhea and often associated with biopsy-defined celiac disease. Two patients with lymphocytic colitis and normal small intestinal biopsies who were administered 40 g of added dietary gluten for four consecutive weeks are presented. Small intestinal biopsies from multiple sites in the proximal small bowel were done after three and four weeks to determine whether pathological changes in latent celiac disease could be induced in these patients with a high gluten-containing diet. In addition, colorectal biopsies were done to determine whether the colitis was sensitive to oral gluten. No alterations in the small intestinal biopsies were detected in either patient and no changes occurred in colitis severity. Although microscopic forms of colitis have been linked to celiac disease, this study indicates that lymphocytic colitis is a heterogeneous clinicopathological disorder that, in some patients, is independent of any gluten-induced intestinal pathological changes.

Biopsy↗
PubMed2001

Familial microscopic colitis.

Collagenous and lymphocytic colitis are two inflammatory conditions of the colon that are often collectively referred to as microscopic colitis. The present report describes what is believed to be the third published case of familial microscopic colitis. A 55-year-old woman who suffered from chronic diarrhea was diagnosed with lymphocytic colitis on colonic biopsy. Subsequently, her 36-year-old daughter was diagnosed with collagenous colitis. The familial occurrence of these diseases may support an immunological hypothesis for their etiology. In addition, it supports the assumption that collagenous and lymphocytic colitis are two manifestations of the same disease process rather than two completely separate entities. The familial tendency of this disease may make a case for early colonoscopy and biopsy in relatives of patients diagnosed with microscopic colitis if they present with suggestive symptoms.

Abdominal Pain↗
PubMed1998

Relationship between fecal bile acids and the occurrence of colorectal neoplasia in experimental murine ulcerative colitis.

OBJECTIVE: The possible role of fecal bile acids in colorectal carcinogenesis in ulcerative colitis has been reported. In this study, we investigated the relationship between fecal bile acids and the occurrence of colorectal neoplasia in experimental murine colitis induced by dextran sulfate sodium. METHODS: Colorectal neoplasia in experimental colitis was induced by dextran sulfate sodium subsequent to a single azoxymethane pretreatment. Fecal bile acids were analyzed by gas-liquid chromatography. RESULTS: Multiple high-grade dysplasias (intramucosal adenocarcinoma) and inflammatory changes were seen in all mice administered dextran sulfate sodium and azoxymethane. Inflammatory changes were also observed in all mice given dextran sulfate sodium only, while neither tumor nor inflammatory changes were detected in any of the control mice. Significant increases in cholic acid were observed in the mice of the colorectal tumor and experimental colitis groups during the experimental period, while in the control mice, no significant changes in fecal bile acids were observed. CONCLUSION: It is suggested that fecal cholic acid and colitis may be intimately related to the development of colorectal neoplasia in this experimental model of murine colitis as well as in ulcerative colitis.

Adenocarcinoma↗
PubMedDate not supplied

Role of endothelins in trinitrobenzene sulfonic acid-induced colitis in rats.

To determine the role of endothelins (ET) on experimental colitis, following intracolonic trinitrobenzene sulfonic acid administration, rats were given orally either bosentan (BS), a nonselective ET receptor antagonist (100 mg/kg in 5% arabic gum), or arabic gum by gavage for 2 or 14 days. Macroscopic damage scores obtained in the vehicle (1.4+/-0.4), acute (4.8+/-0.6) and chronic (3.8+/-0.3) colitis groups were significantly higher than in the control group (0). BS treatment reduced the scores in both acute (3+/- 0.5) and chronic (2.3+/-0.5) colitis groups. Myeloperoxidase (MPO) activities of colonic tissues were elevated in acute and chronic colitis groups (325.1+/-44.9 and 431.8+/-54.6 U/g wet weight) as compared with the control group (73.6+/-11 U/g wet weight). Plasma protein oxidation levels were found to be significantly increased in the chronic colitis group (1,158.1+/-63.4 nmol/ml) compared with the control, ethanol and acute colitis groups (274.3+/-23.1, 490+/-52.2 and 422.2+/-50.5 nmol/ml). BS treatment significantly reduced both the protein oxidation level (375.5+/-46.9 nmol/ml) and MPO activity (167.5+/-35.8 U/g wet weight). The results of the present study suggest the involvement of ETs in the pathogenesis of colonic injury in this animal model of colitis.

Analysis of Variance↗
PubMed1998

Colitis-induced changes in the level of trace elements in rat colon and other tissues.

Trace elements constitute important prosthetic groups in a number of antioxidant enzymes which neutralize free radicals generated during inflammatory conditions such as colitis. However, the status of trace elements in colitis remains to be found. In the present study the concentrations of zinc, copper, manganese and selenium in the colon, liver and serum of rats with acetic acid (HAc)- or trinitrobenzenesulfonic acid (TNBS)-induced colitis were measured using atomic absorption spectrophotometer. Myeloperoxidase and glutathione peroxidase activities were measured spectrophotometrically. Our results show that the selenium concentration was significantly decreased by 33 and 37.5% in the colon and 69 and 78% in liver by HAc and TNBS treatment, respectively. Similarly the zinc concentration in the colon was decreased by 21 and 28% by HAc- and TNBS-induced colitis as compared to the controls, but manganese and copper, remained unaltered. The serum concentrations of copper, zinc and selenium also remained unaltered during colitis. The weight of HAc-treated rats did not decrease while there was a significant weight loss in the TNBS-treated rats. Myeloperoxidase activity was increased, whereas glutathione peroxidase activity was significantly decreased in the colon inflamed by HAc or TNBS as compared to the controls. These findings suggest that colitis induces a reduction in the tissue levels of trace elements which is independent of the way colitis is induced. Our findings of a reduction in Se and glutathione peroxidase activity together suggest that the reduction in the trace element concentrations is not due to dietary factors or malabsorption. The decrease may severely affect the antioxidant potential of the colon and therefore is a putative factor for the progression of disease.

Acetic Acid↗
PubMed2002

Antisense inhibition of cyclooxygenase-2 causes a selective suppression of the Na+-H+ exchanger isoform 3 in rat kidney in experimental colitis.

BACKGROUND: Experimental colitis induces the expression of Na+-H+ exchanger (NHE) isoforms 1 and 3 in the rat colon, however, their status in rat kidney is not established. OBJECTIVES: The renal cortical NHE-1 and -3 expression was examined in the colitic rats. Since cyclooxygenase-2 (cox-2) plays an important role in inflammation, its regulatory role on these isoforms was also investigated by using a cox-2-selective phosphorothioated antisense oligonucleotide (S-oligo). METHODS: Male Sprague-Dawley rats having colitis induced by acetic acid or trinitrobenzenesulfonic acid (TNBS) were given injection of S-oligo (3 mg/kg, i.p.) and a mismatched control oligonucleotide (C-oligo) daily 2 h before inducing colitis. Colonic myeloperoxidase activity (MPO) was used to indicate colitis. The renal cortical levels of NHE-1, NHE-3 and alpha-actin, an internal control, were estimated by the Western blot analysis. RESULTS: Colonic MPO activity was increased and urine output was decreased in both models of colitis. Serum, but not the renal cortical level of TNF-alpha, was increased in both cases. Only TNBS condition showed an increased PGE2 level and a decreased body weight. Water intake and renal histology remained unchanged in either case. The NHE-3 protein, localized on the proximal tubules, was increased significantly without any change in NHE-1 and alpha-actin in both cases. These changes, except the body weight, were significantly reversed by the S-oligo. CONCLUSIONS: Selective induction of NHE-3 and TNF-alpha, and their reversal by cox-2 inhibition, suggest a cox-2-dependent regulation of NHE-3, which possibly involves TNF-alpha released from the site of inflammation and not from the kidney in colitis. The induction of NHE-3 is independent of the nature of colitides, and might be important to compensate for the loss of electrolyte and water in experimental colitis.

Acetic Acid↗
PubMed2002

Inhibition of intestinal bacterial translocation with rifaximin modulates lamina propria monocytic cells reactivity and protects against inflammation in a rodent model of colitis.

BACKGROUND: A modification of the intestinal flora and an increased bacterial translocation is a common finding in patients with inflammatory bowel disease as well as in animal model of colitis. Rifaximin, a non-absorbable derivative of rifamycin, is an effective antibiotic that acts by inhibiting bacterial ribonucleic acid synthesis. AIMS: In the present study, we investigated the effect of the administration of rifaximin (10, 30 and 50 mg/kg/day) or prednisolone (10 mg/kg/day) in 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. METHODS: Colitis was induced in mice by intrarectal administration of TNBS (1.5 mg/mouse in 50% ethanol) and disease severity assessed clinically and by histologic scoring of colon damage, determination of interleukin (IL)-2, IL-12, interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha (protein and mRNA and myeloperoxidase (MPO) activity in the colon. Cytokines production by the lamina propria mononuclear cells (LPMC) and luminal bacteria were also measured. RESULTS: Rifaximin administration (30 or 50 mg/kg/day) increased survival rates of colitic mice and reduced colitis severity as demonstrated by improvement of wasting syndrome, histologic scores, decrease in colon IL-2, IL-12, IFN-gamma and TNF-alpha (protein and mRNA) levels, and diminished colon MPO activity. Rifaximin administration caused a significant reduction of colon bacterial translocation towards mesenteric lymph nodes. LPMC obtained from rifaximin-treated mice released significantly lower amount of IFN-gamma in response to ex vivo stimulation with agonistic anti-CD3 and anti-CD28 antibodies. Rifaximin (50 mg/kg/day) significantly accelerates recovery in mice with established colitis. CONCLUSIONS: Luminal bacterial microflora plays a role in the pathogenesis of TNBS-induced colitis in mice. Rifaximin administration reduces the development of colitis and accelerates healing of established disease by preventing bacterial translocation.

Acute Disease↗
PubMed1977

HLA antigens and ulcerative colitis in Japan.

The HLA antigens in 44 cases of ulcerative colitis and 271 control individuals in Japan were studied. The NIH tissue typing method was used according to the new leukocyte nomenclature adapted by the WHO Committee. In normal Japanese populations, the HLA antigens, which were of high frequency, were HLA A2(37.3%), A9(60.9%) and B5 (40.6%). On the contrary, the significantly high frequency of HLA B5 was demonstrated in ulcerative colitis, compared with that in control. Moreover, HLA B5 in cases with ulcerative colitis excluding those with proctitis only, was found with higher frequency than that in total cases. Although the most frequent haplotype was HLA A9-B5 in control, so frequent haplotype was not found in ulcerative colitis. A family study revealed no significant diathesis on the hapolytpe of HLA in ulcerative colitis. The relationship between MLC locus and ulcerative colitis was not yet clarified from the study of one family whose two members suffered from ulcerative colitis.

Adult↗
PubMed1992

Effects of phosphatidylcholine and phosphatidylinositol on acetic-acid-induced colitis in the rat.

The therapeutic effects of exogenous phosphatidylcholine and phosphatidylinositol on acetic acid-induced colitis in rats were evaluated. A uniform colitis developed 4 days after instillation of 4% acetic acid for 15 s in an excluded colonic segment, also resulting in a 6-fold increase in mucosal permeability. Instillation of 12.5 mg phosphatidylcholine once daily from the day after acetic acid instillation and for the following 2 days prevented partially the development of colitis causing partial mucosal restoration. By increasing the phosphatidylcholine dose to 25 and 50 mg, a better preventive effect was achieved. By starting the phosphatidylcholine instillation immediately after the acetic acid exposure, almost complete prevention of the colitis could be obtained. Similarly, 50 mg phosphatidylinositol in each instillation with the first administration immediately after acetic acid administration resulted in complete prevention of the colitis and a significant decrease in mucosal permeability expressed as a plasma exudation into the colonic lumen. Similar results were obtained when phosphatidylcholine was administered immediately after acetic acid, but the drug then had to be applied twice daily. In contrast, a single application of the same total dose (150 mg) of the two different phospholipids, either 30 min before or immediately after acetic acid administration, could not prevent the development of colitis. It is concluded that both phosphatidylcholine and phosphatidylinositol have a therapeutic effect on the development of acetic acid-induced colitis in the rat.

Acetates↗
PubMed1994

Can 99Tcm HMPAO leucocyte scintigraphy distinguish between Crohn's disease and ulcerative colitis?

This paper has retrospectively analysed the ability of 99Tcm HMPAO leucocyte scintigraphy to distinguish Crohn's disease from ulcerative colitis. The diagnostic criteria were established by reviewing 99Tcm HMPAO leucocyte scintigrams in 123 patients with histologically proven Crohn's disease (83) or ulcerative colitis (40). Uptake in the right iliac fossa with or without other segments of colon, irregular bowel uptake, small bowel uptake or colonic activity with rectal sparing were all strongly suggestive of Crohn's disease. Left sided colitis was found to indicate ulcerative colitis. Total colitis occurred in both ulcerative colitis and Crohn's disease. The criteria were later tested in an additional 62 patients with excellent results (accuracy 98%). In 63 patients in whom the results of barium radiology were also available, the accuracy of scintigraphy was higher (93% and 83%, respectively). We conclude that 99Tcm HMPAO leucocyte scintigraphy can accurately distinguish between Crohn's disease and ulcerative colitis in a large proportion of cases and appears to be more reliable than conventional radiology.

Barium Sulfate↗
PubMed1975

Fibercolonoscopy for the diagnosis of granulomatous colitis.

In order to clarify the significance of fibercolonoscopy in diagnosis of granulomatous colitis, the pathological, radiological, endoscopic and clinical differences between granulomatous colitis and ulcerative colitis were investigated on 12 cases of granulomatous colitis and 23 cases of ulcerative colitis, which underwent colonic resections between 1954 and 1973. The comparative studies have revealed considerable differences in their characteristic features besides the overlapping spectrum. As a consequence of assessments made of the various diagnostic techniques as to usefulness in differential diagnosis between the two colitis conditions, it was noted that fibercolonoscopy and biopsy under direct vision, when applied in conjunction with the conventional procedures, readily facilitate the differential diagnosis without any surgical intervention in all aspects, excepting the depth of inflammatory involvement and the presence of lymphangiectasia. However, the depth of the inflammed lesion as well as lymphangiectasia can also be estimated indirectly. Therefore, it seems that it is possible to make the differential diagnosis between the two colitis conditions even prior to colectomy, with the exception of atypical forms which represent overlapping findings.

Abscess↗
PubMed1998

A practical guide to the management of distal ulcerative colitis.

This article reviews the role of corticosteroids, sulfasalazine and mesalazine (5-aminosalicylic acid, mesalamine), immunosuppressive agents and alternative novel drugs for the treatment of distal ulcerative colitis. Short cycles of traditional, rectally administered corticosteroids (methylprednisolone, betamethasone, hydrocortisone) are effective for the treatment of mild to moderately active distal ulcerative colitis. In this context, their systemic administration is limited to patients who are refractory to either oral 5-amino-salicylates, topical mesalazine or topical corticosteroids. Of no value in maintaining remission, the long term use of either or topical corticosteroids may be hazardous. A new class of topically acting corticosteroids [budesonide, fluticasone, beclomethasone dipropionate, prednisolone-21-methasulphobenzoate, tixocortol (tixocortol pivalate)] represents a valid alternative for the treatment of active ulcerative colitis, and may be useful in the treatment of refractory distal ulcerative colitis. Although there is controversy concerning dosage or duration of therapy, oral and topical mesalazine is effective in the treatment of mild to moderately active distal ulcerative colitis. Sulfasalazine and mesalazine remain the first-choice drugs for the maintenance therapy of distal ulcerative colitis. Evidence exists showing a trend to a higher remission rate with higher doses of oral mesalazine. Topical mesalazine (suppositories or enemas) also is effective in maintenance treatment. For patients with chronically active or corticosteroid-dependent disease, azathioprine and mercaptopurine are effective in reducing either the need for corticosteroids or clinical relapses. Moreover, they are effective for long term maintenance remission. Cyclosporin may be useful in inducing remission in patients with acutely severe disease who do not achieve remission with an intensive intravenous regimen. Existing data suggest that azathioprine and mercaptopurine may be effective in prolonging remission in these patients. The role of alternative drugs for the treatment of distal ulcerative colitis and its different forms is reviewed. In particular data are reported concerning the effectiveness of 5-lipoxygenase inhibitors, topical use of short chain fatty acids, nicotine, local anaesthetics, bismuth subsalicylate enema, sucralfate, clonidine, free radical scavengers, heparin and hydroxychloroquine.

Administration, Oral↗
PubMed1983

Pregnancy in ulcerative colitis.

The course of pregnancy in 97 women with ulcerative colitis was studied over a 12-year period. During this period they had 173 pregnancies and delivered 136 children. There were two gemellary deliveries. Nine women had a spontaneous and 16 an induced abortion, of which 4 were performed on therapeutic indication. For a woman with ulcerative colitis the risk of an exacerbation of the bowel disease was 32% per year in her fertile years, whereas it was 34% per year during pregnancy. This difference is not statistically significant. As compared with women with an inactive bowel disease, women in whom the disease was active at the start of pregnancy had a small but significantly greater risk of spontaneous abortion and premature delivery. The frequency of malformations, prematurity, and neonatal hyperbilirubinaemia was not higher in the children of ulcerative colitis mothers than in those of healthy mothers. Treatment with sulphasalazine, salazosulphadimidine, and corticosteroids had no influence on the course and outcome of pregnancy. Birth length and weight of the children of mothers with ulcerative colitis equalled those for children of healthy mothers. In conclusion, pregnancy does not necessitate any change in the usual medical treatment of ulcerative colitis. Women with ulcerative colitis should be advised preferably to conceive at a time when their bowel disease is inactive. Generally, ulcerative colitis constitutes no indication for induced abortion.

Abortion, Induced↗
PubMed1995

Serum nitrate levels in ulcerative colitis and Crohn's disease.

BACKGROUND: Nitric oxide is an important mediator in inflammatory and autoimmune-mediated tissue destruction and may be of pathophysiologic importance in inflammatory bowel disease. We studied whether serum levels of nitrate, the stable end-product of nitric oxide, are increased in active Crohn's disease or ulcerative colitis, in comparison with quiescent disease and healthy controls. The setting was the gastroenterology unit of the Free University Hospital, Amsterdam. METHODS: In 146 patients--75 with ulcerative colitis and 71 with Crohn's disease--and 33 controls serum nitrate was measured by the Griess reaction after enzymatic conversion of nitrate to nitrite with nitrate reductase. RESULTS: Median serum nitrate concentrations did not differ statistically significantly between ulcerative colitis (median, 34.2 mumol/l; range, 15.6-229.4 mumol/l), Crohn's disease (median 32.3 mumol; range 13.2-143.2 mumol/l), and healthy controls (median, 28.7 mumol/l; range, 13.0-108.4 mumol/l). However, when active ulcerative colitis patients (median, 44 mumol/l; range, 29.1-229.4 mumol/l were compared with inactive ulcerative colitis patients (median, 31.2 mumol/l; range, 15.6-59.7 mumol/l), a significant difference in nitrate concentration was found (p < 0.0001). A significant positive correlation was found between serum nitrate levels in ulcerative colitis and erythrocyte sedimentation rate (ESR) (r = 0.30, p - 0.01), leucocyte count (r = 0.27, p = 0.02), and thrombocyte count (r = 0.24, p = 0.04). Comparing active Crohn's disease patients (median, 37.5 mumol/l; range, 13.2-143.2 mumol/l) with inactive Crohn's disease patients (median, 31.3 mumol/l; range, 14.5-92.3 mumol/l) also showed a significant difference in serum nitrate concentration (p < 0.009). Serum nitrate levels correlated with the ESR (r = 0.26, p = 0.028) and serum albumin (r = 0.38, p = 0.004) as well. CONCLUSION: Nitric oxide production is increased in both active ulcerative colitis and Crohn's disease and may be implicated in the pathogenesis of inflammatory bowel disease.

Adult↗
PubMed1997

Evaluation of the role of neutrophils in the pathogenesis of acetic acid-induced colitis in mice.

BACKGROUND: Neutrophils are thought to play a role in the pathogenesis of inflammatory bowel diseases (IBD) such as ulcerative colitis and Crohn's disease, since prominent neutrophil infiltration has been observed in the inflamed colonic mucosa of patients with IBD. However, the role of neutrophils in the pathogenesis of IBD and experimental colitis remains equivocal. The aim of the present study is to clarify the possible role of neutrophils in the progression of acetic acid-induced colitis in mice. METHODS: Using neutropenic mice treated with cyclophosphamide or with an LTB4 receptor antagonist, ONO-4057, the relationship between the severity of macroscopic colonic damage, the extent of myeloperoxidase (MPO) activities in the colonic tissues, and the number of neutrophils in the blood were examined after induction of colitis in mice. RESULTS: Changes of MPO activity in the colonic tissues paralleled well with the severity of the mucosal damage. In spite of a significant reduction in the number of neutrophils in the blood in cyclophosphamide-treated mice, neither the severity of mucosal damage in the colon nor the increase in MPO activities in the colonic tissues was affected 24 h after induction of colitis. Treatment with ONO-4057 significantly suppressed both the severity of mucosal damage in the colon and MPO activities in the colonic tissues in acetic acid-induced colitis in mice. CONCLUSIONS: The present results, obtained using treatment with cyclophosphamide and ONO-4057, show that the severity or the progression of acetic acid-induced colitis in mice was not influenced by a reduction of circulating neutrophils to about 25% of base line.

Acetic Acid↗
PubMed2005

Hypoxia-inducible factor 1 alpha and vascular endothelial growth factor overexpression in ischemic colitis.

AIM: To examine the etiology and pathophysiology in human ischemic colitis from the viewpoint of ischemic factors such as hypoxia-inducible factor 1 alpha (HIF-1 alpha and vascular endothelial growth factor (VEGF). METHODS: Thirteen patients with ischemic colitis and 21 normal controls underwent colonoscopy. The follow-up colonoscopy was performed in 8 patients at 7 to 10 d after the occurrence of ischemic colitis. Biopsy samples were subjected to real-time RT-PCR and immunohistochemistry to detect the expression of HIF-1 alpha and VEGF. RESULTS: HIF-1 alpha and VEGF expression were found in the normal colon tissues by RT-PCR and immunohistochemistry. HIF-1 alpha and VEGF were overexpressed in the lesions of ischemic colitis. Overexpressed HIF-1 alpha and VEGF RNA quickly decreased to the normal level in the scar regions at 7 to 10 d after the occurrence of ischemic colitis. CONCLUSION: Constant expression of HIF-1 alpha and VEGF in normal human colon tissue suggested that HIF-1 alpha and VEGF play an important role in maintaining tissue integrity. We confirmed the ischemic crisis in ischemic colitis at the molecular level, demonstrating overexpression of HIF-1 alpha and VEGF in ischemic lesions. These ischemic factors may play an important role in the pathophysiology of ischemic colitis.

Case-Control Studies↗
PubMed2005

Favorable response to subcutaneous administration of infliximab in rats with experimental colitis.

AIM: To investigate the influence of infliximab (Remicade) on experimental colitis produced by 2,4,6,trinitrobenzene sulfonic acid (TNBS) in rats. METHODS: Thirty-six Wistar rats were allocated into four groups (three groups of six animals each and a fourth of 12 animals). Six more healthy animals served as normal controls (Group 5). Group 1: colitis was induced by intracolonic installation of 25 mg of TNBS dissolved in 0.25 mL of 50% ethanol and infliximab was subcutaneously administered at a dose of 5 mg/kg BW; Group 2: colitis was induced and infliximab was subcutaneously administered at a dose of 10 mg/kg BW; Group 3: colitis was induced and infliximab was subcutaneously administered at a dose of 15 mg/kg BW; Group 4: colitis was induced without treatment with infliximab. Infliximab was administered on d 2-6. On the 7(th) d, all animals were killed. The colon was fixed in 10% buffered formalin and examined by light microscopy for the presence and activity of colitis and the extent of tissue damage. Tumor necrosis factor-alpha (TNF-alpha) and malondialdehyde (MDA) were also measured. RESULTS: Significant differences concerning the presence of reparable lesions and the extent of bowel mucosa without active inflammation in all groups of animals treated with infliximab compared with controls were found. Significant reduction of the tissue levels of TNF-alpha in all groups of treated animals as compared with the untreated ones was found (0.47+/-0.44, 1.09+/-0.86, 0.43+/-0.31 vs 18.73+/-10.53 respectively). Significant reduction in the tissue levels of MDA was noticed in group 1 as compared to group 4, as well as between groups 2 and 4. CONCLUSION: Subcutaneous administration of infliximab reduces the inflammatory activity as well as tissue TNF-alpha and MDA levels in chemical colitis in rats. Infliximab at a dose of 5 mg/kg BW achieves better histological results and produces higher reduction of the levels of TNF-alpha than at a dose of 10 mg/kg BW. Infliximab at a dose of 5 mg/kg BW produces higher reduction of tissue MDA levels than at a dose of 15 mg/kg BW.

Animals↗