A novel mechanism of chronic intestinal inflammation. Bowel Dis 19, 246—253 2013. Moss, Farzad Ebrahimi, Brishti Biswas, Golam Mostafa, Kathryn T. He is the author or co-author of more than 230 publications including chapters in major medical texts. This book can be recommended to both researchers interested in basic aspects of inflammatory bowel disease and clinical gastroenterologists who want to raise their awareness of the mechanisms underlying clinical manifestations.
His research focuses on the role of cytokine signalling in inflammatory bowel diseases and colon cancer, as well as the pathways that regulate T cell death. Interleukin-23 drives intestinal inflammation through direct activity on T cells. This groundbreaking study defines cytokines as therapeutic targets in chronic intestinal inflammation. Mucosal healing in inflammatory bowel diseases: a systematic review. We recommend that you upgrade to a newer version or to a different web browser. He then joined the University of Erlangen-Nürnberg, Germany, where he is currently Director of the Medical Clinic 1 Gastroenterology, Pneumology, Endocrinology. Absence of a role for interleukin-13 in inflammatory bowel disease.
The immunology of mucosal models of inflammation. The animal models of inflammatory bowel disease provide a framework to define the immunopathogenesis of intestinal inflammation. Eston, Sayeda Nasrin Alam, Angela K. Greenberger is a past President of the American Gastroenterological Association, the American College of Physicians, the Central Society for Clinical Research and the Association of Professors of Medicine. Loss of interleukin-10 signaling and infantile inflammatory bowel disease: implications for diagnosis and therapy. Chen, Kanakaraju Kaliannan, Halim Yammine, Sonoko Narisawa, José Luis Millán, H.
Interleukin-23 restrains regulatory T cell activity to drive T cell-dependent colitis. The transcription factor T-bet regulates mucosal T cell activation in experimental colitis and Crohn's disease. Kinetics of in vitro response to interferon γ inducers. Host-microbe interactions have shaped the genetic architecture of inflammatory bowel disease. . Interleukin-2- and interferon-γ-secreting T cells in normal and diseased human intestinal mucosa.
Notwithstanding the high cost involved, these biological therapies show a high index of remission, enabling a significant reduction in cases of surgery and hospitalization. T-cell abnormalities in inflammatory bowel disease are mediated by interleukin 2. This study identifies cytokines as a link between inflammation and tumour growth in experimental models of colitis. In ulcerative colitis, there are several therapies available, depending on the stage of the disease. This trusted text is known world-wide for its thorough coverage of procedures and techniques in endoscopy and treating various liver disorders. To obtain the best experience, we recommend you use a more up to date browser or turn off compatibility mode in Internet Explorer.
Studies in these models support the hypothesis that exaggerated immune responses to normal enteric microflora are involved in the initiation and perpetuation of chronic intestinal inflammation. Antibodies to interleukin 12 abrogate established experimental colitis in mice. European Crohn's and Colitis Organisation meeting, Copenhagen, 2014. Interferon-β-1a for the treatment of steroid-refractory ulcerative colitis: a randomized, double-blind, placebo-controlled trial. Induction of intestinal Th17 cells by segmented filamentous bacteria. This article highlights innate lymphoid cells as key cytokine producers in experimentally induced colitis. Long-term complications, extraintestinal manifestations, and mortality in adult Crohn's disease in population-based cohorts.
This book broadly treats the topics that lead to understanding of the pathogenesis of this disease in an organized, systematic approach. Hodin, Intestinal alkaline phosphatase has beneficial effects in mouse models of chronic colitis , Inflammatory Bowel Diseases , 17 , 2 , 532-542 , 2011. Thank you for visiting nature. Subclinical intestinal inflammation in patients with Crohn's disease following bowel resection: a smoldering fire. Functional modulation of Crohn's disease myofibroblasts by anti-tumor necrosis factor antibodies.