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PubMed2005

Increased lymphocyte trafficking to colonic microvessels is dependent on MAdCAM-1 and C-C chemokine mLARC/CCL20 in DSS-induced mice colitis.

Although enhanced lymphocyte trafficking is associated with colitis formation, little information about its regulation is available. The aim of this study was to examine how the murine liver and activation-regulated chemokine (mLARC/CCL20) contributes to lymphocyte recruitment in concert with vascular adhesion molecules in murine chronic experimental colitis. T and B lymphocytes isolated from the spleen were fluorescence-labelled and administered to recipient mice. Lymphocyte adhesion to microvessels of the colonic mucosa and submucosa was observed with an intravital microscope. To induce colitis, the mice received two cycles of treatment with 2% dextran sodium sulphate (DSS). In some of the experiments antibodies against the adhesion molecules or anti-mLARC/CCL20 were administered, or CC chemokine receptor 6 (CCR6) of the lymphocytes was desensitized with excess amounts of mLARC/CCL20. Significant increases in T and B cell adhesion to the microvessels of the DSS-treated mucosa and submucosa were observed. In chronic colitis, the accumulation of lymphocytes was significantly inhibited by anti-mucosal addressin cell adhesion molecule (MAdCAM)-1 mAb, but not by anti-vascular cell adhesion molecule-1. In DSS-treated colonic tissue, the expression of mLARC/CCL20 was significantly increased, the blocking of mLARC/CCL20 by monoclonal antibody or the desensitization of CCR6 with mLARC/CCL20 significantly attenuated the DSS-induced T and B cell accumulation. However, the combination of blocking CCR6 with MAdCAM-1 did not further inhibit these accumulations. These results suggest that in chronic DSS-induced colitis, both MAdCAM-1 and mLARC/CCL20 may play important roles in T and B lymphocyte adhesion in the inflamed colon under flow conditions.

Animals↗
PubMed2001

Immunomodulation of experimental colitis: the role of NK1.1 liver lymphocytes and surrogate antigens--bystander effect.

The imbalance between Th1 pro-inflammatory and Th2 anti-inflammatory cytokine-producing cells plays a major role in the pathogenesis of inflammatory bowel disease (IBD). Induction of oral tolerance to colitis-extracted proteins was previously shown to down-regulate the anti-colon immune response, thereby alleviating experimental colitis. Immune bystander effect and liver-associated lymphocytes expressing the NK1.1 marker (NK1.1(+) LAL) have been suggested as being important in tolerance induction. The aims of the present study were to determine whether oral administration of inflammatory and non-inflammatory colon-extracted proteins of different species can induce peripheral immune tolerance and alleviate experimental colitis; and to examine the role of NK1.1(+) LAL in oral tolerance induction. Colitis was induced in C57/B6 mice by intracolonic instillation of trinitrobenzene sulphonic acid (TNBS). Mice received six oral doses of colonic proteins extracted from TNBS-colitis colonic wall, or normal colonic wall, from four different species. Standard clinical, macroscopic, and microscopic scores were used for colitis assessment. Serum interferon gamma (IFNgamma) and interleukin 10 (IL10) levels were measured by ELISA. To evaluate the role of NK1.1(+) LAL in maintaining the balance between immunogenic and tolerogenic subsets of cells, their cytotoxicity functions were tested in tolerized and non-tolerized-mice. The administration of mouse-derived colitis-extracted proteins, or of surrogate proteins extracted from normal mouse colon, or from rat or human inflammatory colons, was found to alleviate experimental colitis. Tolerized mice had less diarrhoea; showed a marked reduction of colonic ulceration, intestinal and peritoneal adhesions, wall thickness, and oedema; and demonstrated a significant improvement of all microscopic parameters for colitis. Induction of tolerance led to an increase in IL10 and a decrease in IFNgamma serum levels. NK1.1(+) LAL cytotoxicity function increased markedly in tolerized mice. In contrast, mice fed with proteins extracted from normal rat, rabbit, and human colon, or from rabbit inflammatory colon, developed severe colitis, with a marked increase in IFNgamma and a decrease in IL10 serum levels, and down-regulation of NK1.1(+) LAL function. This study has shown that oral tolerance can be induced in experimental colitis by means of the feeding of surrogate antigens; this alleviates experimental colitis. NK1.1(+) LAL cytotoxicity function is associated with peripheral tolerance induction and may help to maintain the Th1/Th2 immune balance.

Animals↗
PubMed1990

Prevention of Clostridium difficile-induced experimental pseudomembranous colitis by Saccharomyces boulardii: a scanning electron microscopic and microbiological study.

The ability of Saccharomyces boulardii to protect mice against intestinal pathology caused by toxinogenic Clostridium difficile was studied. Different regions of the intestine of experimental mice were prepared for observation by scanning electron microscopy or homogenized for C. difficile enumeration and quantification of toxin A by enzyme immunoassay and toxin B by cytotoxicity. The test group was treated for 6 d with an S. boulardii suspension in drinking water and challenged with C. difficule on day 4. The three control groups were: axenic mice, mice treated with only S. boulardii and mice only challenged with C. difficile. The results showed that: (i) 70% of the mice infected by C. difficile survived when treated with S. boulardii; (ii) the C. difficile-induced lesions on the small and large intestinal mucosa were absent or markedly less severe in S. boulardii-treated mice; and (iii) there was no decrease in the number of C. difficile but rather a reduction in the amount of toxins A and B in S. boulardii-treated mice.

Animals↗
PubMedDate not supplied

Associated ulcerative colitis, sclerosing cholangitis, and insulin-dependent diabetes mellitus.

We report two young men with clinical and laboratory evidence of macroscopic ulcerative colitis, sclerosing cholangitis, and insulin-dependent diabetes mellitus. The first patient presented at age 15 with vomiting, abdominal pain, weight loss, and abnormal liver function test results. Liver biopsy and endoscopic retrograde cholangiopancreatography (ERCP) demonstrated sclerosing cholangitis. Colonoscopy with biopsy revealed ulcerative colitis which responded to sulfasalazine. Diabetes occurred at age 18 and insulin therapy was begun. The second patient was 19 at presentation with diarrhea, hematochezia, and weight loss. Proctosigmoidoscopy revealed ulcerative colitis, and sulfasalazine led to clinical remission. Three months later he developed diabetes requiring insulin therapy. At age 28, he developed elevated alkaline phosphatase, and ERCP revealed sclerosing cholangitis. At age 37 he expired from adenocarcinoma that metastasized to the liver. Literature review revealed only one possible case report of this association with microscopic asymptomatic ulcerative colitis in that patient. Statistical analysis suggests that this association is real rather than a chance occurrence. An autoimmune process may be involved and a specific histocompatibility locus antigen (HLA) type may exert a regulatory influence.

Adolescent↗
PubMedDate not supplied

Is histology useful for the assessment of the efficacy of immunosuppressive agents in IBD and if so, how should it be applied ?

Crohn's disease and ulcerative colitis are two chronic relapsing inflammatory bowel diseases of unknown etiology. Both conditions are characterized by a considerable morbidity and have an impact upon the social and economic aspects of the patients life. At present, medical treatment is mainly aiming at the control of the inflammation. Drugs used for ulcerative colitis can induce microscopic healing of the mucosa. Similar results have been obtained recently with immunomodulatory drugs in Crohn's disease. The cost of these drugs is however high and the use of these drugs can be associated with side effects. Furthermore, many of the drugs need to be given for a long period. Therefore it is appropriate to assess the efficacy of the drugs before commercial use and even when used in routine practice. For both ulcerative colitis and Crohn's disease, clinical parameters combined in indices and endoscopy are commonly used together with some laboratory tests for the assessment of disease activity. In ulcerative colitis, histology has been used along with the other instruments for the measurement of disease activity because it was shown that the mucosal lesions could improve. More recently, histology has also been used for Crohn's disease. Routinely, disease activity when assessed with microscopy, should be divided into mild, moderate and severe. For drug trials and study purposes, more objective scoring systems should be used. Preferentially, a generally accepted score is used. This allows comparisons between different studies. Different scoring systems have been designed for ulcerative colitis and Crohn's disease. For the latter, multiple biopsies should be analysed. Most scoring systems still need validation.

Biopsy↗
PubMed2004

Extensive intestinal spirochaetosis in pigs challenged with Brachyspira pilosicoli.

A field isolate of Brachyspira pilosicoli, the aetiological agent of porcine intestinal spirochaetosis, was inoculated by stomach tube into six 6-week-old pigs. All animals developed loose to watery faeces and were killed successively on days 8, 14 or 17 post-inoculation (day 17 being the end of the study). Mild mucosal reddening and flecks of pus characterized the gross lesions, while diffuse, catarrhal colitis was revealed microscopically in all animals. Intestinal spirochaetosis with moderate to densely packed end-attached B. pilosicoli organisms was revealed extensively on the mucosal surface of the large intestines by light microscopy and fluorescent in situ hybridization. This study is the first to report extensive intestinal spirochaetosis in pigs challenged with B. pilosicoli.

Animals↗
PubMed2001

Amelioration of immune-mediated experimental colitis: tolerance induction in the presence of preexisting immunity and surrogate antigen bystander effect.

Oral tolerance is a recognized procedure for induction of antigen-specific peripheral immune hyporesponsiveness. Recently, it has been shown that oral tolerance can be used to prevent experimental colitis. The aim of this study was to test whether induction of oral tolerance toward proteins extracted from inflammatory and noninflammatory colons can alleviate preexisting experimental colitis. Colitis was induced in BALB/c mice by intracolonic instillation of 2,4,6-trinitrobenzenesulfonic acid (TNBS). Mice received five oral doses of colonic proteins extracted from TNBS-induced colitis or normal colons, before, or 7 days after colitis was induced. Standard clinical, macroscopic, and microscopic scores were used for colitis assessment. Serum interferon gamma (IFNgamma) and interleukin (IL)4 levels were measured by enzyme-linked immunosorbent assay. Feeding of colitis- or normal colon-extracted proteins before, or following colitis induction, ameliorated colonic inflammation as shown by decreased diarrhea, increased body weight, reduction of colonic ulcerations, intestinal and peritoneal adhesions, wall thickness, and edema. Histological parameters for colitis were markedly improved in tolerized animals, and there was a significant reduction in inflammatory response and mucosal ulcerations. Tolerized mice developed an increase in IL4 and a decrease in IFNgamma serum levels. The results show that induction of oral tolerance to colitis- or normal colon-extracted proteins down-regulated preexisting anticolon immune response, thereby ameliorating experimental colitis. Tolerance induction was mediated via a shift from a proinflammatory T helper (Th)1 to an anti-inflammatory Th2 immune response.

Animals↗
PubMed2005

[Histopathology of ulcerative colitis in biopsy].

For histologic diagnosis on biopsy specimens, we gave an outline of macroscopic and microscopic features of ulcerative colitis (UC), including differential diagnosis. The most important histologic features on biopsy are dense mixed inflammatory infiltrate in the lamina propria mucosae, mucosal architectural abnormality, and vascular change. Evidence of colorectal adenocarcinoma, dysplasia, and cytomegalovirus infection should also be taken into account. Although diagnostic criteria for UC are well understood, the biopsy diagnosis of UC is comparatively difficult. Thus the diagnosis of UC should be made mainly by clinical pictures, course of the illness, and radiological and endoscopic pictures.

Biopsy↗
PubMed2001

Chronic use of non-steroidal anti-inflammatory drugs does not alter colonic mucosa of patients without diarrhoea.

BACKGROUND: Several types of colitis can be NSAID-induced, but whether chronic use of NSAIDs alters colonic mucosa in patients without diarrhoea is not known. PATIENTS AND METHODS: Biopsy specimens of rectal mucosa were taken in six patients with rheumatoid arthritis without diarrhoea receiving NSAIDs (group 1, n=6). Patients with rheumatoid arthritis without diarrhoea not receiving NSAIDs (group 2, n=9), and patients undergoing surveillance colonoscopy (group 3, n=23) served as controls. In all patients from the three study groups, intraepithelial lymphocyte count and apoptotic cell count were assessed, and sub-epithelial collagen band thickness was measured. Leucocyte population of lamina propria was evaluated semi-quantitatively. HLA-DR and CD25 expression of mucosal cells was appreciated by immunohistochemistry. RESULTS: Intraepithelial lymphocyte count was in the normal range in all three group patients, and not statistically different between groups. Apoptotic epithelial cell count was not different between groups. Sub-epithelial collagen band thickness was normal in all the patients. No patient had a marked infiltration of lamina propria by leucocytes, and HLA-DR and CD25 were normally expressed in all patients. CONCLUSION: These results from a small sample of patients suggest that patients without diarrhoea receiving NSAIDs on a long-term basis do not develop microscopic or inflammatory colitis.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1986

Salmonella osteomyelitis in a rhesus monkey.

An adult male rhesus monkey (Macaca mulatta) developed clinical signs of severe osteomyelitis of the left femur 42 days after onset of enteritis. Salmonella sp. were cultured from feces, blood, and femoral lesions. Response to antibiotic therapy was poor, and the animal was euthanized. The left femur, with pathologic fracture and involucrum, and the right femur, tibia and fibula were most severely affected. Additionally hepatic microgranulomas, mild tubulointerstitial nephritis, medullary histiocytosis and erythrophagocytosis in the lymph nodes, and a mild colitis were diagnosed microscopically. The severity of the disease and serum electrophoresis findings were suggestive of lowered resistance to the organism, possibly due to anemia or polychlorinated biphenyl toxicosis.

Animals↗
PubMedDate not supplied

Large intestine obstruction complicated with perforation: a rare manifestation of Schistosoma mansoni infection.

The authors report a case of a 25 year old Brazilian man with a history of crampy abdominal pain in the left iliac fossa for 2 weeks, abdominal distention, mucous diarrhea and anorexia. The patient presented signs of hemodynamic instability and a hard mass palpated in the left iliac fossa presented peritoneal irritation. At laparotomy, fecal peritonitis and a punched-out perforation of the midsigmoid colon were found. A left hemicolectomy was performed with terminal colostomy. Specimen examination revealed a thickened rectosigmoid wall, narrow lumen and multiple mucosal polyps. Microscopically, chronic granulomatous colitis with Schistosoma mansoni eggs confirmed the etiology. To the authors' knowledge, this is the first case of obstruction complicated with perforation due to mansoni schistosomiasis reported in the literature.

Adult↗
PubMed2001

Classification of Brachyspira spp. isolated from Swedish dogs.

Brachyspira spp. were isolated from 21 of 32 sampled dogs (66%) in a colony of Swedish beagle dogs with a history of diarrhea and from 3 of 17 Swedish pet dogs (17%) with diarrhea. All Swedish isolates were weakly beta-hemolytic and gave a negative indole reaction. Eighty-eight percent showed negative alpha-galactosidase and hippurate reactions, but a positive beta-glucosidase reaction. Two isolates were hippurate positive with a negative beta-glucosidase reaction. One additional German isolate diverged by showing a positive indole reaction in combination with a positive hippurate reaction. Sequencing of 16S rDNA indicated that the hippurate-positive isolates belonged to the species Brachyspira pilosicoli. Four representative isolates were examined using pulsed-field gel electrophoresis (PFGE) and compared with six reference strains and five porcine isolates of Brachyspira spp. The canine isolates clustered together in the PFGE analysis. Necropsy examination of a culture-positive B. pilosicoli colony-raised beagle dog revealed macro- and microscopical lesions of colitis with numerous spiral-shaped bacteria in the lumens of the crypts, in goblet cells and within the colonic epithelium.

Animals↗
PubMed1994

Yersinia enterocolitica: an inducer of chronic inflammation.

The aim of the present study was to elucidate the connection between yersiniosis and chronic inflammation. During the period 1974-83, Yersinia enterocolitica infection was diagnosed in 458 hospitalized patients by antibody response, or isolation. The patients were followed for 4-14 years (1987); 160 were readmitted with chronic disease. Fifty-three patients had persistent joint complaints, 18 developed ankylosing spondylitis, 14 rheumatoid arthritis, and 17 iridocyclitis. Thirty-eight patients suffered from chronic abdominal pain, and another 28 from chronic diarrhoea. Two who underwent proctocolectomy microscopically had ulcerative colitis. Eleven patients developed neurological disease; others developed conditions such as chronic nephritis, thyroid disease, insulin-dependent diabetes, etc. Chronic hepatitis, found in 22 patients, was significantly correlated with positive test for antinuclear antibody and rheumatoid factor, and with death. Several patients developed chronic multiorgan disease, probably with chronic hepatitis as pivot. Regarding the whole material, the difference between observed and expected cumulative survival rates remained significant for 8 years (0.9189 < 0.9456; p < 0.025), indicating a substantial impact on long-term survival exerted by chronic yersiniosis.

Adolescent↗
PubMed2003

Pancreatic changes in TNBS-induced colitis in mice.

BACKGROUND AND AIM: Recent clinical data suggest that pancreatitis could be an extraintestinal manifestation of inflammatory bowel disease. However, no experimental data support such a clinical relationship. The aim of this study was to investigate the presence of pancreatic damages in mice with TNBS-induced colitis. METHODS: Colitis was induced in Balb/C mice by intrarectal instillation of TNBS. Control mice received either intrarectal instillation of NaCl saline solution or 50% ethanol. Presence of colitis was assessed by macroscopic and microscopic examination, extent of mucosal damage being evaluated by the scoring systems of Wallace and Ameho in 8 mice with TNBS-induced colitis and in 4 controls. Pancreatic samples from the same mice underwent morphological examination after standard coloration. Intrapancreatic expression of the pancreatitis-associated protein (PAP), a marker of pancreatic inflammation, was monitored by automated immunohistochemistry using specific antibodies. In addition, quantification of TNFalpha mRNA by competitive PCR and semi-quantification of PAP, IL-10 and IL-1B mRNAs were performed on pancreas in 10 mice with TNBS-induced colitis and in 10 control mice. RESULTS: All mice treated with TNBS and none of the controls had colitis. Macroscopic and microscopic examination of the pancreas of the 4 control mice was normal, whereas in 5 out of the 8 TNBS-treated mice histological changes were observed, with inflammatory infiltrate and fibrin aggregates at the periphery of the gland. PAP immunohistochemistry was negative in all control mice and positive in all mice with TNBS-induced colitis, with a patchy distribution of staining. PAP immunolocalized to the cytoplasm of acinar cells, duct cells and islets of Langherans being negative. PAP and IL-1B mRNA levels in the pancreas were significantly increased but the increase in TNFalpha mRNA level did not reach statistical significance (P=0.06). IL-10 mRNA levels did not show any significant modification. CONCLUSION: PAP overexpression in pancreas demonstrates that inflammatory stress early occurs in the mouse pancreas during the course of TNBS-induced colitis. The concomitant pancreatic overexpression of IL-1B and, to a lesser extent, of TNFalpha, two proinflammatory cytokines also associated with the intestinal lesions of colitis, supported a pancreatic inflammatory mechanism mediated by cytokines.

Animals↗
PubMed2006

Colitis-induced oxidative damage of the colon and skeletal muscle is ameliorated by regular exercise in rats: the anxiolytic role of exercise.

Epidemiological studies have shown that exercise protects the gastrointestinal tract, reducing the risk of diverticulosis, gastrointestinal haemorrhage and inflammatory bowel disease, while many digestive complaints occurring during exercise are attributed to the adverse effects of exercise on the colon. In order to assess the effects of regular exercise on the pathogenesis of colitis, Sprague-Dawley rats of both sexes were either kept sedentary or given exercise on a running wheel (0.4 km h(-1), 30 min for 3 days week(-1)). At the end of 6 weeks, under anaesthesia, either saline or acetic acid (4%, 1 ml) was given intracolonically. Holeboard tests were performed for the evaluation of anxiety at 24 h before and 48 h after induction of colitis. Increased 'freezing time' in the colitis-induced sedentary group, representing increased anxiety, was reduced in the exercised colitis group (P < 0.05). On the third day following the colonic instillation, the rats were decapitated under brief ether anesthesia and the distal 8 cm of the colons were removed. In the sedentary colitis group, macroscopic and microscopic damage scores, malondialdehyde level and myeloperoxidase activity were increased when compared to the control group (P < 0.01-0.001), while exercise prior to colitis reduced all the measurements with respect to sedentary colitis group (P < 0.05-0.001). The results demonstrate that low-intensity, repetitive exercise protects against oxidative colonic injury, and that this appears to involve the anxiolytic effect of exercise, suggesting that exercise may have a therapeutic value in reducing stress-related exacerbation of colitis.

Animals↗
PubMed2001

Beneficial effects of glycocholic acid (GCA) on gut mucosal damage in bile duct ligated rats.

In order to investigate the effect of bile acids on gastrointestinal inflammations, bile duct ligated rats (BDL) were treated with GCA (25 mM/ml, oral or colonic) or saline I h before ethanol challenge and twice daily for 3 days in the ileitis group, while GCA was given twice daily for 3 days in the colitis group. BDL reduced the macroscopic and microscopic damage scores in the ileitis group compared to sham operated group, while it had no significant effect on ulcer or colitis groups. However, GCA given in BDL group reduced the ulcer index and microscopic damage in colitis group compared to saline-treated groups, but had no effect in ileitis group. Both BDL and GCA administration in BDL group reduced ileitis- or colitis-induced elevations in MPO levels. GCA administration in BDL group inhibited gastric acid output and volume. Our results suggest that oral or colonic administration of primary bile acids may be useful for the treatment of gastrointestinal inflammations.

Animals↗