Kucharzik Torsten, Maaser Christian, Lügering Andreas, Kagnoff Martin, Mayer Lloyd, Targan Stephan, Domschke Wolfram
Department of Medicine B, University of Münster, Münster, Germany.
Inflamm Bowel Dis. 2006 Nov;12(11):1068-83. doi: 10.1097/01.mib.0000235827.21778.d5.
The inflammatory bowel diseases (IBD) are comprised of two major phenotypes, Crohn's disease (CD) and ulcerative colitis (UC). Research over the last couple of years has led to great advances in understanding the inflammatory bowel diseases and their underlying pathophysiologic mechanisms. From the current understanding, it is likely that chronic inflammation in IBD is due to aggressive cellular immune responses to a subset of luminal bacteria. Susceptibility to disease is thereby determined by genes encoding immune responses which are triggered by environmental stimuli. Based on extensive research over the last decade, there are several new and novel pathways and specific targets on which to focus new therapeutics. The following review summarizes the current view on the four basic tenets of the pathophysiological basis of IBD and its implications for therapies of IBD: genetics, immune dysregulation, barrier dysfunction and the role of the microbial flora.
炎症性肠病(IBD)包括两种主要类型,即克罗恩病(CD)和溃疡性结肠炎(UC)。过去几年的研究在理解炎症性肠病及其潜在病理生理机制方面取得了巨大进展。根据目前的认识,IBD中的慢性炎症可能是由于对一部分管腔细菌的强烈细胞免疫反应所致。疾病易感性由此由编码免疫反应的基因决定,这些免疫反应由环境刺激触发。基于过去十年的广泛研究,有几个新的途径和特定靶点可作为新疗法的重点。以下综述总结了目前关于IBD病理生理基础的四个基本原则及其对IBD治疗的意义的观点:遗传学、免疫失调、屏障功能障碍以及微生物群的作用。