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PubMed2005

Interleukin-5 potentiates the growth response of Caco-2 cells to IGF-II: a role in colonic carcinogenesis complicating ulcerative colitis?

UNLABELLED: Longstanding ulcerative and Crohn's colitis increases the risk of colorectal cancer (CRC) compared to the general population. Elevated IGF-II mRNA and protein have been found in tumour tissue in sporadic CRC. The association of IGF-II in colitis-related-CRC is unknown. OBJECTIVES: To determine whether pro-inflammatory cytokines associated with colitis, namely IL-5, TNF-alpha and IL-1beta, alter the proliferative effect of IGF-II on the colorectal cancer cell line, Caco-2. DESIGN: Caco-2 cells were cultured with IGF-II and IL-5, TNF-alpha or IL-1beta. At 24 h intervals cell proliferation was assessed. The mechanism of action of any synergistic affect was investigated by RT-PCR to determine change in mRNA expression of IGF-II, IGF-1R or IGF-2R. RESULTS: After 72 h, IGF-II increased absorption (corresponding to cell density) compared to controls by 25% (p < 0.02). Co-incubation with IGF-II and IL-5 increased absorption by 42% (p < 0.001) compared to controls and 18% (p < 0.03) compared to IGF-II alone. Enhanced growth response was also seen with TNF-alpha and IL-1beta, but less so than IL-5. The IL-5 receptor was not expressed by Caco-2 cells and mRNA expression of the IGF-1R or IGF-2R was unchanged by incubation with cytokines. CONCLUSIONS: IGF-II promotes Caco-2 growth, an effect enhanced with IL-5, TNF-alpha and IL-1beta. The greatest response was with IL-5. This was IL-5 receptor-independent. Possible mechanisms include IL-5 interaction on an un-identified receptor or interference with IGF-binding proteins, as occurs with IL-1beta and IL-6. The enhanced growth response of Caco-2 cells to pro-inflammatory cytokines and IGF-II may have implications for the pathogenesis of CRC formation in colitis.

Caco-2 Cells↗
PubMed2002

Significance of appendiceal involvement in patients with ulcerative colitis.

BACKGROUND: The appendix is occasionally involved in patients with distal ulcerative colitis. This study investigated the clinical significance of patchy involvement at the appendiceal orifice in ulcerative colitis. METHODS: Colonoscopy was performed in 40 patients with active distal ulcerative colitis of mild to moderate severity. Patients were divided into 2 groups based on the presence or absence (positive or negative) of involvement at the appendiceal orifice at colonoscopy. Clinical activity, histologic grade of inflammation, and subsequent clinical course were compared between patients who were positive (appe(+)) and negative (appe(-)). RESULTS: Twenty-three patients had involvement at the appendiceal orifice (reddish mucosa with mucinous exudate). The proximal-most extent of involvement by ulcerative colitis, the endoscopic grade, and clinical activity were not different between appe(+) and appe(-) groups. However, histologic grade of inflammation in the ascending colon was higher in the appe(+) group than in the appe(-) group. The endoscopic remission rate at 12 months was higher in the appe(+) group than in the appe(-) group (84% vs. 40%, p < 0.05). CONCLUSIONS: In patients with distal ulcerative colitis, involvement at the appendiceal orifice may be indicative of histologically active disease, which responds reasonably well to pharmacotherapy.

Adolescent↗
PubMed2003

Upper lobe fibrosis in ulcerative colitis.

We report a case of ulcerative colitis where chest radiograph and high-resolution computed tomography (HRCT) of the lungs revealed bilateral upper lobe fibrosis, which was misdiagnosed and treated as pulmonary tuberculosis. The diagnosis of ulcerative colitis was confirmed by sigmoidoscopy and rectal biopsy.

Colitis, Ulcerative↗
PubMed2001

Characterization of antigen-presenting dendritic cells in the peripheral blood and colonic mucosa of patients with ulcerative colitis.

OBJECTIVE: Increased lymphocyte activation and production of inflammatory cytokines are implicated in the pathogenesis of ulcerative colitis. Because antigen-presenting dendritic cells play a cardinal role in the activation and survival of activated lymphocytes, the aim of the present study was to characterize dendritic cells in ulcerative colitis. DESIGN: This study was designed to compare the phenotypes and functions of peripheral blood dendritic cells among healthy normal volunteers and patients with ulcerative colitis or Crohn's disease. Activated dendritic cells were also localized at the colonic mucosa. METHODS: Peripheral blood dendritic cells were generated from 15 patients with ulcerative colitis, 10 patients with Crohn's disease and 15 healthy control volunteers. The stimulatory capacities of dendritic cells were analysed in an allogenic mixed lymphocyte reaction. Nitric oxide was detected by the Griess method. Single- and dual-colour flow cytometry was employed to study the levels of maturation of dendritic cells. Activated dendritic cells were localized immunohistochemically in the colonic mucosa. RESULTS: In comparison to normal controls, peripheral blood dendritic cells from patients with ulcerative colitis showed significantly increased stimulatory capacities (P < 0.05) and produced significantly higher levels of nitric oxide (P < 0.05). The numbers of activated dendritic cells were also significantly higher in ulcerative colitis (P < 0.05). Mature and activated dendritic cells expressing the CD83 antigen were detected at the inflamed colonic mucosa in patients with ulcerative colitis and Crohn's disease. CONCLUSIONS: Activated and mature dendritic cells may have a role in the induction of an exacerbated immune response in ulcerative colitis. This study provides the scientific and logical basis for blocking the maturation and activation of dendritic cells in ulcerative colitis as a new therapeutic intervention.

Adult↗
PubMed2000

A reproducible grading scale for histological assessment of inflammation in ulcerative colitis.

BACKGROUND: Evaluation of histological activity in ulcerative colitis needs to be reproducible but has rarely been tested. This could be useful both clinically and in clinical trials. AIM: To develop reproducible criteria which are valid in the assessment of acute inflammation (activity) and chronicity, and to evaluate these features in an interobserver variability study. METHODS: A six grade classification system for inflammation was developed which could also be fine tuned within each grade. The grades were: 0, structural change only; 1, chronic inflammation; 2, lamina propria neutrophils; 3, neutrophils in epithelium; 4, crypt destruction; and 5, erosions or ulcers. Ninety nine haematoxylin-eosin sections from endoscopically inflamed and non-inflamed mucosa from patients with distal ulcerative colitis were assessed in two separate readings by three pathologists independently and without knowledge of the clinical status. Interobserver agreement was compared pairwise using kappa statistics. RESULTS: Initially, kappa values between the observers were 0.20, 0.42, and 0.26, which are too low to be of value. Following development of a semiquantitative pictorial scale for each criterion, kappa values improved to 0.62, 0.70, and 0.59. For activity defined by neutrophils between epithelial cells, kappa values were 0.903, 1.000, and 0.907. Complete agreement was reached in 64% of samples of endoscopically normal and in 66% of endoscopically inflamed tissue. Neutrophils in epithelium correlated with the presence of crypt destruction and ulceration. CONCLUSION: A histological activity system was developed for ulcerative colitis that showed good reproducibility and modest agreement with the endoscopic grading system which it complemented. It has potential value both clinically and in clinical trials.

Biopsy↗
PubMed1978

Isolation and characterization of colonic tissue-bound antibodies from patients with idiopathic ulcerative colitis.

To determine if specific anticolon antibodies bound to colonic mucosa occur in ulcerative colitis, we obtained surgical specimens of colon from five patients with ulcerative colitis, one patient with diverticulitis, and three control subjects with carcinoma. Two specimens of ileum and cecum were also obtained from patients with Crohn ileocolitis. Tissue was homogenized and washed and bound Ig was eluted by citrate buffer, pH 3.2. Concentrated eluates of all specimens from patients with ulcerative colitis reacted with antisera to kappa and gamma and not with antisera to alpha and mu chains. Corresponding eluates from all other specimens did not react with these antisera, but did react with antialbumin. The presence of IgG in ulcerative colitis eluates was also determined by immunoelectrophoresis, immunocoprecipitation, and affinity chromatography with antisera against human IgG. Indirect immunofluorescence and uptake of radiolabeled antibody demonstrated antigenic sites in diseased colonic epithelium of biopsy specimens obtained from six additional patients with ulcerative colitis and three patients with idiopathic proctitis, but not in patients with Crohn disease, nonspecific diarrhea, and bacillary dysentery and control subjects. Although the role of colitis colon-bound antibody in the pathogenesis of ulcerative colitis is unclear, local antibody-antigen complexes may initiate colonic epithelial cytolysis by various immunologically mediated mechanisms.

Autoantibodies↗
PubMed2000

Total antioxidant capacity of colon in patients with chronic ulcerative colitis.

It has been proposed that oxidative stress is involved in the pathophysiology of ulcerative colitis. We have reported the depletion of the nonenzymatic antioxidant, glutathione, in colon from active and inactive ulcerative colitis. The colon contains several biochemically linked antioxidant systems. We hypothesized that diminished total antioxidant capacity in active ulcerative colitis would be associated with increased colonic lipid peroxidation. This study was designed to determine total antioxidant capacity and lipid hydroperoxide levels using colon obtained at surgery from controls (N = 16; 4 females, 12 males; mean age 70 years), and active and inactive ulcerative colitis (N = 15; 3 females, 12 males; mean age 39). Total antioxidant capacity of control colon was higher in muscularis externa compared to the mucosal-submucosal layer (P < 0.05). There were no differences in colonic total antioxidant capacity or lipid hydroperoxide levels comparing control colon to inactive and active ulcerative colitis. The results did not support depletion of tissue total antioxidant capacity by free radicals. Depletion of glutathione in ulcerative colitis may be a specific disorder rather than a secondary defect attributable to global oxidative stress. Nonspecific antioxidant supplements appear unlikely to be beneficial in the treatment of ulcerative colitis.

Adult↗
PubMed1990

Lack of association between oral contraceptive use and ulcerative colitis.

Previous epidemiological studies suggesting an association between oral contraceptive use and ulcerative colitis incidence have been weak and conflicting. To measure a possible association, 46 incident cases of ulcerative colitis patients, women aged 18-50 years, were compared with peer-nominated age-matched and sex-matched controls. There were no differences between case and control patients in demographic characteristics. There was no association between oral contraceptive use and ulcerative colitis (current use: odds ratio 0.70, 95% confidence interval 0.27-1.83; former use: odds ratio 1.14, confidence interval 0.41-3.15; current or former use: odds ratio 0.86, confidence interval 0.40-1.85). Stratifying by disease location (pancolitis or left-sided disease) also failed to identify an association. Controlling for possible confounding effects of cigarette smoking did not alter the lack of association between oral contraceptive use and ulcerative colitis. Similarly, testing for interaction failed to demonstrate any effect modification. Analyzing for duration of current oral contraceptive use or time interval since last use failed to demonstrate a "dose-response" effect. The study was of sufficient size to detect statistical significance for oral contraceptive use for odds ratios of 2.8 and higher. In this matched case-control study of incident cases and community controls, there was no association between oral contraceptive use and ulcerative colitis incidence. To date, there is no evidence suggesting that women predisposed to the development of ulcerative colitis should be advised to avoid oral contraceptive use.

Adult↗
PubMedDate not supplied

Coexistence of celiac disease and ulcerative colitis.

Coexistence of celiac disease and ulcerative colitis has been reported from Western countries. We report two patients, a 30-year old man and a 16-year old boy, who presented initially with features of celiac disease and later developed ulcerative colitis.

Adolescent↗
PubMed2005

[Extraintestinal complications in patients with ulcerative colitis].

Extraintestinal complications of patients with ulcerative colitis contribute to quality of life and mortality of the patients. Extraintestinal complications involve many organ systems. Skin, mucocutaneous, hepatobiliary, and joints complications are major extraintestinal complications. Some disorders correspond the activity of the colitis, other complications develop independently of the bowel inflammation. The purpose of this review is to update the clinicians concerning the etiology, clinical course and the therapy of the extraintestinal manifestations associated with ulcerative colitis.

Cholangitis, Sclerosing↗
PubMed1994

Appendectomy protects against ulcerative colitis.

BACKGROUND/AIMS: Defining risk factors for ulcerative colitis (UC) is important to better understand the pathogenesis of this idiopathic disease. One factor modulating the disease is smoking. A pilot study showed the absence of appendectomy in the medical history of patients with ulcerative colitis. The aim of the present case control study was to compare the relative risk of developing UC after appendectomy with the relative risk of developing UC with an intact appendix. METHODS: One hundred seventy-four (84 females and 90 males, mean age 34.9 years) consecutive UC patients examined at our inflammatory bowel disease clinic or hospital ward, were included. Fifty-six had pancolitis (32%) and 118 (68%) suffered from left-sided colitis. The control group consisted of 161 consecutive patients examined at the orthopedic clinic (86 females and 75 males, mean age 40.9 years). RESULTS: Two parameters, absence of appendectomy and smoking, were closely related to the development of UC. Before the onset of UC, only 1 of the 174 patients (0.6%) had undergone an appendectomy. Of the 161 controls, 41 (25.4%) had undergone an appendectomy. The difference between the two groups was highly significant with an odds ratio of 59.1 (95% CI, 18-189; P < 0.001). The relative risk of getting the disease associated with nonsmoking was 2.95 (95% CI, 1.69-5.17). CONCLUSIONS: Appendectomy is a protective factor against UC.

Adolescent↗
PubMed1979

Carcinoid tumour as a complication of ulcerative colitis.

Patients with long-standing ulcerative colitis have an increased chance of developing a carcinoma of the colon, especially when the inflammatory process involves the entire colon, but no case of a carcinoid tumour of the colon occurring in a patient with ulcerative colitis has been reported.

Carcinoid Tumor↗
PubMed1997

New ulcerative colitis model induced by sulfhydryl blockers in rats and the effects of antiinflammatory drugs on the colitis.

We tried to produce a new ulcerative colitis model in rats by topical administration of sulfhydryl blockers. After male SD rats were fasted for 24 hr, 100 microliters of 3% N-ethylmaleimide (NEM) or iodoacetamide (IA) was introduced into the colon via a Nelaton's catheter. Both NEM and IA caused severe diarrhea with rectal bleeding and decreased body weight for about 7 days. At autopsy, adhesions and dilatation of the colon and severe mucosal lesions were observed. Both the weight and myeloperoxidase activity of the colon increased markedly. Maximum changes were observed within 1-3 days followed by gradual recovery, but even on day 21, some abnormalities were still observed. The ulceration and inflammation of the colon were confirmed by histological studies. Antiinflammatory drugs such as indomethacin inhibited the inflammation of the colon by NEM, but aggravated the ulceration. These results revealed that sulfhydryl blockers instilled into the colon caused ulcerative colitis in the rat. This model may be useful in studies on the pathogenesis of ulcerative colitis and the evaluation of drugs for therapy. Furthermore, it was suggested that antiinflammatory drugs may delay the healing of colonic ulcers.

Animals↗
PubMed2002

Relationship between the platelet activating factor acetylhydrolase gene and intractability of ulcerative colitis.

PURPOSE: Platelet activating factor, which is a potent mediator of inflammatory injury in ulcerative colitis, is inactivated by platelet activating factor acetylhydrolase. Recently, a point mutation (G994 to T transversion) was observed in exon 9 of the platelet activating factor acetylhydrolase gene, and this mutation was found to be associated with a decrease in platelet activating factor acetylhydrolase activity in plasma. The aim of this study was to determine whether the gene mutation was associated with the severity of ulcerative colitis. METHODS: We studied 53 patients with ulcerative colitis and 108 control subjects. The plasma platelet activating factor acetylhydrolase genotype was determined as representative cases with three different genotypes (GG, GT, and TT) by an allele-specific polymerase chain reaction. RESULTS: There was no significant difference in genotypic frequency (GG, GT, and TT genotype frequencies were 68, 30, and 2 percent in controls and 55, 45, and 0 percent in ulcerative colitis patients). Platelet activating factor acetylhydrolase activity in plasma was also measured and did not differ significantly between ulcerative colitis patients and controls (1.50+/-0.12 vs. 1.81+/-0.34 nmol/min/50 microl, P = 0.60). However, according to the relationship between the platelet activating factor acetylhydrolase gene mutation and clinical characteristics of ulcerative colitis patients, the operative ratio cause of unresponsiveness to steroid therapy was significantly higher in patients with the GT genotype than in those with the GG genotype (66.7 vs. 27.6 percent, P = 0.019). CONCLUSION: We conclude that steroid-nonresponsive ulcerative colitis patients have a high frequency of the platelet activating factor acetylhydrolase gene mutation. Therefore, genotyping of this gene may be a useful marker to predict responsiveness to steroid therapy.

Adult↗
PubMed2001

Upper gastrointestinal mucosal disease in pediatric Crohn disease and ulcerative colitis: a blinded, controlled study.

BACKGROUND: Upper gastrointestinal endoscopic biopsies often show histologic abnormalities in Crohn disease. Consequently, it has been proposed that routine endoscopy could help to distinguish Crohn disease from ulcerative colitis. Surprisingly, however, recent case reports and an uncontrolled study suggested that similar abnormalities may occur in ulcerative colitis. Therefore, a blinded, controlled study was performed. METHODS: Esophageal, gastric antral, and duodenal biopsies from children with Crohn disease (n = 28) and ulcerative colitis (n = 14) were compared with those from controls undergoing endoscopy for suspected reflux esophagitis (n = 22). Two pathologists, unaware of patient identity and diagnosis, agreed on a consensus report. Severity of inflammation was scored semiquantitatively. Helicobacter pylori colonization was an exclusion criterion. RESULTS: Inflammation was reported as follows: esophagitis: controls 91%; Crohn disease: 72%; ulcerative colitis: 50%; gastritis: controls: 27%; Crohn disease: 92% (P < 0.001); ulcerative colitis: 69%; duodenitis: controls: 9%; Crohn disease: 33%; ulcerative colitis: 23%. In Crohn disease, granulomas were noted in 40% of patients (P = 0.001). Duodenal cryptitis was noted in 26% of patients with Crohn disease but not ulcerative colitis. In one patient with ulcerative colitis, neutrophilic infiltration of gastric glands was seen. Abnormalities seen in Crohn disease and ulcerative colitis included gastroduodenal ulceration (Crohn disease, 7%; ulcerative colitis, 8%), villus atrophy (Crohn disease, 11%; ulcerative colitis, 15%), and increased intraepithelial lymphocytes (Crohn disease, 15%; ulcerative colitis, 31% [P < 0.05]). None of these abnormalities was noted in the controls. CONCLUSION: Although the presence of granulomas can support a diagnosis of Crohn disease, severe inflammation and other abnormalities occur in the proximal gastrointestinal tract in Crohn disease and ulcerative colitis.

Adolescent↗
PubMed2005

Activation of nuclear factor kappaB in colonic mucosa from patients with collagenous and ulcerative colitis.

BACKGROUND AND AIMS: Expression of inducible nitric oxide synthase (iNOS) is greatly upregulated in the colonic mucosa of patients with collagenous and ulcerative colitis. As the transcription factor nuclear factor kappaB (NFkappaB) is a major inducer of iNOS gene expression, we compared activation and transcriptional activity of NFkappaB in colonic mucosal biopsies from these patients. PATIENTS: Eight patients with collagenous colitis, six with relapsing ulcerative colitis, and eight with uninflamed bowel were studied. METHODS: NFkappaB DNA binding activity was assessed by electrophoretic mobility shift assay and inhibitor of NFkappaB (IkappaB) kinase (IKK) activity by immunocomplex kinase assay. In vivo recruitment of NFkappaB to the iNOS promoter was determined by chromatin immunoprecipitation analysis and transcriptional activity by NFkappaB gene expression profiling arrays. Cells showing NFkappaB activation were identified by immunohistochemistry. RESULTS: In collagenous and ulcerative colitis, as opposed to uninflamed bowel, IKKbeta activity and strong NFkappaB DNA binding gave rise to activation of identical NFkappaB subunits and recruitment of transcriptionally active p65 to the iNOS promoter. In collagenous colitis, activated NFkappaB was observed only in epithelial cells while up to 10% of lamina propria macrophages showed activation in ulcerative colitis. CONCLUSIONS: In collagenous and ulcerative colitis, colonic mucosal NFkappaB is activated and recruited to the iNOS promoter in vivo via an IKKbeta mediated pathway. As collagenous colitis is not associated with tissue injury, these data challenge the prevailing view that activation of NFkappaB per se mediates tissue injury. Our results suggest that downstream inflammatory reactions leading to tissue damage originate in lamina propria immune cells, as increased NFkappaB activity in collagenous colitis was localised solely in epithelial cells, but present also in macrophages in ulcerative colitis.

Colitis, Collagenous↗
PubMed1999

Birth-cohort phenomenon in the time trends of mortality from ulcerative colitis.

It has been suggested that the mortality trends of ulcerative colitis in England and Wales are shaped by an underlying birth-cohort phenomenon. This pattern implies that exposure to an environmental risk factor early in life plays a crucial role in the development of the disease. The authors tested whether the birth-cohort pattern is unique to British mortality statistics or a common feature of ulcerative colitis in western countries by using the vital statistics from England and Wales, Canada, Scotland, Switzerland, The Netherlands, and the United States. Ulcerative colitis death rates from the six countries were plotted against the periods of death or periods of birth. Mortality from ulcerative colitis increased in successive generations born throughout the second half of the 19th century. It peaked in subjects born between 1880 and 1890 and has declined since then. Strikingly similar patterns were found in the six countries and when women and men were analyzed separately. The birth-cohort pattern indicates that development of ulcerative colitis is strongly influenced by one or several environmental risk factors, which act during a short period early in life. In western countries, exposure to this risk has changed in a similar fashion.

Age Distribution↗