Interleukin-17 mRNA in active inflammatory bowel disease

Hendel, Jakob; Feddersen, Kurt; Kirman, Irena; Nielsen, Ole Haagen

doi:10.1016/s0016-5085(98)84040-7

Cited by 61 publications

(73 citation statements)

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“…In the present study, low or no expression of COX-1 was observed in the CD, actinic colitis and control groups, in agreement with the study of HENDEL and NIELSEN (15) . In contrast, JACKSON et al (17) demonstrated increased expression of COX-1 in the ulcerated borders of the gastric mucosa.…”

Section: A B C Dsupporting

confidence: 93%

Evaluation of the immunoexpression of COX-1, COX-2 and p53 in Crohn's disease

Romero

Artigiani

Costa

et al. 2008

Arq. Gastroenterol.

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-Background -Crohn's disease accompanied by nonspecific or idiopathic ulcerative proctocolitis corresponds to a condition called intestinal inflammatory disease. The immunoexpression of cyclooxygenase 2 (COX-2) in Crohn's disease becomes more marked with progression of the disease and the presence of wild-type p53 suppresses the transcription of COX-2. Aims -To investigate the immunoexpression of cyclooxygenase 1 (COX-1), COX-2 and p53 in Crohn's ileocolitis and to correlated this expression with clinical and histopathological parameters. Methods -Forty-five cases of Crohn's disease, 16 cases of actinic colitis (diseased-control group) and 11 cases without a history of intestinal disease (normal control group) were studied. Hematoxylin-eosin-stained sections were submitted to histopathological analysis and the immunohistochemical expression of COX-1, COX-2 and p53 was evaluated by the streptavidin-biotin-peroxidase method. Results -Sixty percent of the Crohn's disease patients were women and 40% were men, with 75.5% whites and 25.5% non-whites. The disease involved the terminal ileum in 44.5% of cases, ileum in 33.3%, colon in 20% and duodenum-ileum in 2.2%. A significant association was observed between COX-2 immunoreactivity and age ≤40 years. Histopathological analysis of Crohn's disease samples showed mild or moderate crypt distortion (57.8% and 35.6% of cases), atrophy (6.6%), mild, moderate and marked chronic inflammation (46.7%, 26.7% and 20%), acute inflammatory activity (93.3%), ulceration (24.4%), mucin depletion (37.8%), Paneth's cells (24.4%), intraepithelial lymphocytes (93.3%), and subepithelial collagen (6.7%). In the CD group, COX-1 immunoreactivity in epithelial and inflammatory cells was observed in 26.7% and 22.2% of cases, respectively.

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Section: A B C Dsupporting

confidence: 93%

Evaluation of the immunoexpression of COX-1, COX-2 and p53 in Crohn's disease

Romero

Artigiani

Costa

et al. 2008

Arq. Gastroenterol.

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“…Previous observations indicate higher than normal PTGS2 expression in colonic epithelial cells in IBS [6] and that PTGS2 expression is associated with disease activity [7]. In addition to these data our analysis indicates that patients do not responding to IFX therapy may exhibit even higher PTGS expression than those with appropriate response.…”

Section: Discussionsupporting

confidence: 74%

Validation of Biomarkers in Gene Expression Datasets of Inflammatory Bowel Disease: IL13RA2, PTGS2 and WNT5A as Predictors of Responsiveness to Infliximab Therapy

Győrffy¹

2014

J Proteomics Bioinform

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Background: Some patients with inflammatory bowel disease (IBD) do not respond to infliximab (IFX) therapy. Gene expression studies revealed genes that may help to predict non-responding IBD patients. Our purpose was to validate the discriminating power of published genes. Methods:Microarray datasets of IBD patients responding or non-responding to IFX were downloaded from GEO database ('transcriptomic arm'). Published genes discriminating responding and non-responding patients were identified in PubMed ('biomarker arm'). Using ROC-analysis, the discriminating performance of genes in 'biomarker arm' were re-tested in each datasets of 'transcriptomic arm'. We also performed an independent analysis of colon biopsy datasets to identify novel discriminating genes. Results:The transcriptomic arm of four GEO datasets (3 and 1 from colon biopsies and blood cells, respectively) included 99 patients (of those, 59 and 40 were IFX responder and non-responder, respectively). Of the 65 candidate genes reported in biopsy specimens 25 genes discriminated significantly (p<0.05) infliximab responders and nonresponders in the three biopsy datasets consistently. Of the 39 candidate genes reported in peripheral blood 9 genes provided significant discrimination after re-testing. Independent analysis of three biopsy datasets identified the top five genes. Three genes (IL13RA2, PTGS2 and WNT5A) were highly effective discriminator in each analysis. Conclusion:This analysis identified IL13RA2, PTGS2 and WNT5A, three genes in colonic tissues of IBD patients as suitable to discrimination between patients responding and non-responding to IFX therapy. These genes encode proteins implicated in intestinal pathology; the high expression in non-responding patients may indicate important targets in IBD therapy.

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“…31,32 We have demonstrated it in both inflamed and noninflamed mucosa in all stages of neoplastic progression in UC (Figure 1). In addition, some of the actively inflamed nondysplastic areas showed no COX-2 expression (Figure 1).…”

Section: Cox-2 In Uc-associated Neoplasiamentioning

confidence: 83%

The Role of Cyclooxygenase 2 in Ulcerative Colitis-Associated Neoplasia

Agoff

Brentnall

Crispin

et al. 2000

The American Journal of Pathology

150

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Cyclooxygenase 2 (COX-2) overexpression has been described in sporadic colonic neoplasia, but its role in ulcerative colitis (UC) neoplastic progression remains unexplored. Although the specific role of cyclooxygenase in colonic neoplasia is uncertain, its inhibition by nonsteroidal anti-inflammatory drugs decreases the risk of sporadic colonic adenocarcinoma and causes regression of adenomas in familial adenomatous polyposis. To investigate the role of COX-2 in UC-associated neoplasia, we assessed COX-2 protein and mRNA expression throughout the spectrum of UC-associated neoplastic lesions in four total colectomy specimens, using immunocytochemistry and a novel TaqMan reverse transcriptase-polymerase chain reaction assay. The findings were correlated with DNA ploidy and inflammatory activity. We found COX-2 overexpression throughout the neoplastic spectrum in UC (P < 0.0001, R 2 ‫,)35.0؍‬ even in diploid samples that were negative for dysplasia. Overall, neoplastic change explained 53% of the variation in COX-2 expression, whereas inflammatory activity explained only 11%. COX-2 was overexpressed in all aneuploid samples and in 38% of diploid samples (P ‫؍‬ 0.0074). cDNA representational difference analysis was also performed and revealed that COX-2 mRNA was an up-regulated cDNA representational difference analysis difference product. COX-2 overexpression occurs early in UC-associated neoplasia, and the increase cannot be explained by inflammatory activity alone. The data suggest that COX-2-specific inhibitors may have a chemopreventative role in UC but the possibility that they could exacerbate UC inflammatory activity needs to be tested. Cyclooxygenase 1 (COX-1) and cyclooxygenase 2 (COX-2) are cyclooxygenase enzymes that convert arachidonic acid to inflammatory and other physiological mediators, including prostaglandins, prostacyclin, and thromboxane. 1,2 COX-1 is constitutively expressed in most tissues, including the gastrointestinal tract, at a relatively stable level and is thought to help protect the gastrointestinal tract from injury. 1,2 COX-2 is an inducible cyclooxygenase whose production is stimulated by interleukin-1, tumor necrosis factor, and many other mediators. 1,2 COX-2 is thought to play a role in the reparative process after mucosal injury in the gastrointestinal tract. 1,2 Multiple studies suggest that COX-2 plays a role in sporadic colorectal neoplasia, based on its overexpression in colonic adenomas and carcinomas, as shown by both immunohistochemistry and reverse transcriptasepolymerase chain reaction (RT-PCR). [3][4][5] Cyclooxygenase inhibitors such as nonsteroidal anti-inflammatory drugs (NSAIDs) substantially decrease the risk of colorectal cancer, as well as the number and size of adenomas in familial adenomatous polyposis patients. 6 -8 Experimentally, NSAIDs prevent colonic adenocarcinoma in rodents with an familial adenomatous polyposis phenotype (the APC min mouse model). 9,10 Understanding the role of COX-2 in colonic neoplasia is thus particularly important because of these t...

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Interleukin-17 mRNA in active inflammatory bowel disease

Cited by 61 publications

References 0 publications

Evaluation of the immunoexpression of COX-1, COX-2 and p53 in Crohn's disease

Evaluation of the immunoexpression of COX-1, COX-2 and p53 in Crohn's disease

Validation of Biomarkers in Gene Expression Datasets of Inflammatory Bowel Disease: IL13RA2, PTGS2 and WNT5A as Predictors of Responsiveness to Infliximab Therapy

The Role of Cyclooxygenase 2 in Ulcerative Colitis-Associated Neoplasia

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