Wei Jia, Feng Jiexiong
Department of Pediatric Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P R China.
Recent Pat Inflamm Allergy Drug Discov. 2010 Jun;4(2):105-17. doi: 10.2174/187221310791163071.
Inflammatory bowel disease (IBD) consists of Crohn's disease (CD) and ulcerative colitis (UC). It is thought to be caused by genetic, abnormal immune response of the intestinal immune system and dysfunction of intestinal mucosal barrier against enteric bacteria. Mutational genes can affect the development of IBDs via certain signaling pathways. The abnormal signaling pathways play an important role in the inflammatory process and can lead to dysregulation of the inflammatory response and are crucial in the pathogenesis of IBDs. The signaling pathways mainly include P38 MAPK, JNK MAPK, PI3K/Akt, NF-kappaB signaling pathways. Intestinal microorganisms play a key role in the initiation and maintenance of disease. Disorders of signaling pathways including TLR, NF-kappaB can act on the intestinal barrier, and cause uninhibitedly release of effector T cells which are the central cells mediating inflammation in CD. This review highlights relevant patents and a new insight of signaling pathways associated with IBDs will help to develop better therapeutic approaches.
炎症性肠病（IBD）包括克罗恩病（CD）和溃疡性结肠炎（UC）。它被认为是由遗传因素、肠道免疫系统的异常免疫反应以及肠道黏膜屏障对肠道细菌的功能障碍引起的。突变基因可通过某些信号通路影响IBD的发展。异常的信号通路在炎症过程中起重要作用，可导致炎症反应失调，在IBD的发病机制中至关重要。这些信号通路主要包括P38丝裂原活化蛋白激酶（P38 MAPK）、应激活化蛋白激酶（JNK MAPK）、磷脂酰肌醇-3激酶/蛋白激酶B（PI3K/Akt）、核因子κB（NF-κB）信号通路。肠道微生物在疾病的起始和维持中起关键作用。包括Toll样受体（TLR）、NF-κB在内的信号通路紊乱可作用于肠道屏障，导致效应T细胞不受抑制地释放，而效应T细胞是介导CD炎症的核心细胞。本综述重点介绍了相关专利，对与IBD相关的信号通路的新见解将有助于开发更好的治疗方法。
