Karin Michael, Lawrence Toby, Nizet Victor
Laboratory of Gene Expression and Signal Transduction, Department of Pharmacology, UCSD School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093, USA.
Cell. 2006 Feb 24;124(4):823-35. doi: 10.1016/j.cell.2006.02.016.
Clinical and epidemiologic studies have suggested an association between infectious agents and chronic inflammatory disorders and cancer. Better understanding of microbial pattern-recognition receptors and innate immune signaling pathways of the host is helping to elucidate the connection between microbial infection and chronic disease. We propose that a key aspect of pathogenesis is an aberrant epithelial barrier that can be instigated by microbial toxins, environmental insults, or the genetic predisposition of the host. Loss of epithelial integrity results in activation of resident inflammatory cells by microbial invaders or endogenous ligands. When coupled with a failure of normal control mechanisms that limit leukocyte activation, a cascade is established that induces chronic inflammation and its consequences. Here, we outline this mechanistic framework and briefly review how alteration of innate immune response genes in murine models can provide insights into the potential microbial origins of diverse conditions including Crohn's disease, psoriasis, atherosclerosis, diabetes, and liver cancer.
临床和流行病学研究表明,感染因子与慢性炎症性疾病及癌症之间存在关联。对宿主的微生物模式识别受体和固有免疫信号通路的更好理解,有助于阐明微生物感染与慢性疾病之间的联系。我们提出,发病机制的一个关键方面是异常的上皮屏障,它可能由微生物毒素、环境损伤或宿主的遗传易感性引发。上皮完整性的丧失会导致常驻炎症细胞被微生物入侵者或内源性配体激活。当与限制白细胞激活的正常控制机制失效相结合时,就会建立一个级联反应,引发慢性炎症及其后果。在此,我们概述了这一机制框架,并简要回顾了小鼠模型中固有免疫反应基因的改变如何能够为包括克罗恩病、银屑病、动脉粥样硬化、糖尿病和肝癌在内的多种病症的潜在微生物起源提供见解。