Abstract: The present invention relates to methods for predicting acute severe colitis treatment response. Currently, there is no biomarker of drag response. The present invention provides the first prediction tool for responses to first- and second-line treatments in acute severe ulcerative colitis. Putative mRNA targets of dysregulated microRNAs were identified from patient biopsies. One classifier of fifteen colonic microRNAs plus five biological values at admission were identified with a prediction accuracy of 96.6% for discriminating responders from non-responders to steroids. Using a similar method, 6 and 4 mucosal microRNA-based algorithms were identified to classify responders from non-responders to infliximab and cyclosporine.

Abstract: The mucosa is an integrated network of tissues, cells and effector molecules that protect the host from environmental insults and infections. Dysregulation of immunity at mucosal surfaces is thought to lead to mucosal inflammatory diseases such as those affecting the gastrointestinal system (Crohn's disease, ulcerative colitis and irritable bowel syndrome) and respiratory system (asthma, allergy and chronic obstructive pulmonary disorder). Anterior Gradient 2 (AGR2) is a dimeric Protein Disulfide Isomerase (PDI) family member involved in the regulation of protein quality control in the Endoplasmic Reticulum (ER). Its deletion in the mouse intestine increases tissue inflammation and promotes the development of inflammatory bowel disease (IBD). Now the inventors demonstrate that modulation of AGR2 dimer formation yields pro-inflammatory phenotypes notably though the secretion of AGR2 (eAGR2) that promotes monocyte attraction.

Abstract: The present invention relates to methods for predicting acute severe colitis treatment response. Currently, there is no biomarker of drug response. The present invention provides the first prediction tool for responses to first- and second-line treatments in acute severe ulcerative colitis. Putative mRNA targets of dysregulated microRNAs were identified from patient biopsies. One classifier of fifteen colonic microRNAs plus five biological values at admission were identified with a prediction accuracy of 96.6% for discriminating responders from non-responders to steroids. Using a similar method, 6 and 4 mucosal microRNA-based algorithms were identified to classify responders from non-responders to infliximab and cyclosporine.

Abstract: The present invention relates to methods for predicting acute severe colitis treatment response. Currently, there is no biomarker of drug response. The present invention provides the first prediction tool for responses to first- and second-line treatments in acute severe ulcerative colitis. Putative mRNA targets of dysregulated microRNAs were identified from patient biopsies. One classifier of fifteen colonic microRNAs plus five biological values at admission were identified with a prediction accuracy of 96.6% for discriminating responders from non-responders to steroids. Using a similar method, 6 and 4 mucosal microRNA-based algorithms were identified to classify responders from non-responders to infliximab and cyclosporine.

Abstract: The present invention relates to methods and pharmaceutical compositions for the treatment of inflammatory bowel diseases.

Abstract: The present invention relates to methods and pharmaceutical compositions for the treatment of inflammatory bowel diseases. The presents methods relates to a method of treating an inflammatory bowel disease in a subject in need thereof comprising administering the subject with a therapeutically effective amount of at least one OX1R agonist.

Abstract: The present invention relates to methods and pharmaceutical compositions for the treatment of inflammatory bowel diseases. The presents methods relates to a method of treating an inflammatory bowel disease in a subject in need thereof comprising administering the subject with a therapeutically effective amount of at least one OX1R agonist.

Abstract: The present invention relates to methods and kits for diagnosing ulcerative colitis in a subject. In particular, the present invention relates to a method for diagnosing ulcerative colitis in a subject comprising the steps consisting of determining in a sample obtained from the subject the expression level of at least one gene selected from the group consisting of ADH4, ADH6, ADHFE1, AKR1A1, AKR7A2, ALDH1A3, ALDH1L1, ALDH7A1, AOX1, BCHE, CBR3, CES1, CYP1B1, CYP2E1, CYP2W1, CYP4F11, CYP51A1, ESD, KCNAB2, COMT, GSTA4, GSTP1, INMT, MGST2, SULT2A1, TPMT, UGT1A4, UGT1A9, UGT2B7, ABCA1, ABCA2, ABCB1, ABCC1, ABCC10, ABCC5, ABCC6, ABCG2, ATP7A, SLC1A3, SLC7A5, SLC10A2, SLC15A1, SLC15A2, SLC19A2, SLC19A3, SLC22A3, SLC28A3, SLC29A2, SLC38A1, SLC38A5, SLC47A1, SLCO2B1, SLCO4C1, ARNT, FOXO1, HIF3A, NCOA2, NCOR2, NR1H3, NR3C1, PPARD, PPARGC1A, RARB, RXRB, and THRB.

Abstract: The present invention relates to a non human model animal for ulcerative colitis and its main complications such as primary sclerosing cholangitis and colorectal cancer. More particularly, the present invention relates to a transgenic non human animal model for ulcerative colitis and its main complications such as primary sclerosing cholangitis, and colorectal cancer comprising a targeted disruption in the IL10 and NOX1 genes so that IL10 and NOX1 are not expressed in said animal.

Abstract: The present invention relates to a method for classifying an inflammatory bowel disease in a patient as a Crohn's disease or as an ulcerative colitis, said method comprising a step of measuring an expression profile of miRNA in a sample from the patient, wherein said miRNA are miR15a, miR26a, miR29a, miR29b, miR30c, miR126*, miR127-3p, miR-142-3p, miR-142-5p, miR-146a, miR-146b-5p, miR150, miR-181d, miR-182, miR185, miR196a, miR199a-3p, miR199a-5p, miR199b-5p, miR-203, miR223, miR-299-5p, miR320a, miR324-3p, miR-328.

Abstract: The present invention relates to a non human model animal for ulcerative colitis and its main complications such as primary sclerosing cholangitis and colorectal cancer. More particularly, the present invention relates to a transgenic non human animal model for ulcerative colitis and its main complications such as primary sclerosing cholangitis, and colorectal cancer comprising a targeted disruption in the IL10 and NOX1 genes so that IL10 and NOX1 are not expressed in said animal.

Abstract: The present invention relates to a non human model animal for ulcerative colitis and its main complications such as primary sclerosing cholangitis and colorectal cancer. More particularly, the present invention relates to a transgenic non human animal model for ulcerative colitis and its main complications such as primary sclerosing cholangitis, and colorectal cancer comprising a targeted disruption in the IL10 and NOX1 genes so that IL10 and NOX1 are not expressed in said animal.

Abstract: The present invention relates to screening methods and pharmaceutical compositions for the treatment of inflammatory bowel disease. More particularly, the present invention relates to a method for screening a plurality of test substances useful for the prevention or treatment of an inflammatory bowel disease comprising the steps consisting of (a) testing each of the test substances for its ability to restore the integrated stress response and (b) and positively selecting the test substances capable of restoring said integrated stress response. A further aspect of the invention relates to an agent capable of restoring the integrated stress response (ISR) for use in the treatment of an inflammatory bowel disease.

Abstract: The present invention relates to a method for classifying an inflammatory bowel disease in a patient as a Crohn's disease or as an ulcerative colitis, said method comprising a step of measuring an expression profile of miRNA in a sample from the patient, wherein said miRNA are miR15a, miR26a, miR29a, miR29b, miR30c, miR126*, miR127-3p, miR-142-3p, miR-142-5p, miR-146a, miR-146b-5p, miR150, miR-181d, miR-182, miR185, miR196a, miR199a-3p, miR199a-5p, miR199b-5p, miR-203, miR223, miR-299-5p, miR320a, miR324-3p, miR-328.