Relationship between methylation and colonic inflammation in inflammatory bowel disease

AIM: To investigate the relationship between the methylation status in the SLIT2 and TGFB2 promoters and colonic inflammation in inflammatory bowel disease patients. METHODS: We evaluated the methylation status of 2 genes (SLIT2 and TGFB2) in 226 biopsies taken from 62 colonoscopies of 38 patients (29 ulcerative colitis and 9 Crohn's colitis) using methylation-specific melting curve analysis. The relationships between methylation status and clinical, biological, endoscopic and histological activities were evaluated. Twenty-three of the 38 patients had a second colonoscopy and were included in a longitudinal analysis. Numerical results were given as the means ± SD of the sample and range, except when specified. Student t analysis, U Mann Whitney and ANOVA factor were used to compare the means. Qualitative results were based on the χ2 test. RESULTS: SLIT2 methylation was more frequent in samples with endoscopic activity than with endoscopic remission (55% vs 18%, P < 0.001). SLIT2 methylation was also higher in samples with acute inflammation (56.5%) than in samples with chronic (24%) or absent inflammation (15%) (P < 0.001). For TGFB2 methylation, the correlation was only significant with endoscopic activity. Methylation was higher in the distal colon for both genes (P < 0.001 for SLIT2 and P = 0.022 for TGFB2). In the multivariate analysis, only inflammation status (and not disease duration or extension) was independently associated with SLIT2 methylation [OR = 6.6 (95%CI: 1.65-27.36), P = 0.009]. In the longitudinal analysis, the maintenance of endoscopic remission was protective for methylation

Effectiveness of third-class biologic treatment in Crohn's disease : a multi-center retrospective cohort study

C

Bacterial intestinal superinfections in inflammatory bowel diseases beyond Clostridum difficile

Besides genetics and environmental factors, intestinal microbiota seem to play a major role in the pathogenesis of inflammatory bowel diseases. For many decades, it has been said that some enteropathogens may even trigger both inflammatory bowel disease development and disease flares. For this reason, stool testing had been performed in inflammatory bowel disease flares but current guidelines only recommend to rule out Clostridium difficile infection and there is no clear advice for other enteropathogens given that the scarce available evidence points at a low prevalence of this sort of intestinal superinfections with no clear impact on disease course. The present article reviews the current knowledge about the role of bacterial enteropathogens on disease pathogenesis and flares beyond C. difficile