Schmid-Schönbein Geert W
Department of Bioengineering, The Whitaker Institute for Biomedical Engineering, University of California San Diego, La Jolla, California 92093-0412, USA.
Annu Rev Biomed Eng. 2006;8:93-131. doi: 10.1146/annurev.bioeng.8.061505.095708.
In the past, inflammation has been associated with infections and with the immune system. But more recent evidence suggests that a much broader range of diseases have telltale markers for inflammation. Inflammation is the basic mechanism available for repair of tissue after an injury and consists of a cascade of cellular and microvascular reactions that serve to remove damaged and generate new tissue. The cascade includes elevated permeability in microvessels, attachment of circulating cells to the vessels in the vicinity of the injury site, migration of several cell types, cell apoptosis, and growth of new tissue and blood vessels. This review provides a summary of the major microvascular, cellular, and molecular mechanisms that regulate elements of the inflammatory cascade. The analysis is largely focused on the identification of the major participants, notably signaling and adhesion molecules, and their mode of action in the inflammatory cascade. We present a new hypothesis for the generation of inflammatory mediators in plasma that are derived from the digestive pancreatic enzymes responsible for digestion. The inflammatory cascade offers a large number of opportunities for development of quantitative models that describe various aspects of human diseases.
过去,炎症一直与感染及免疫系统相关。但最近的证据表明,更多种类的疾病都有炎症的特征性标志物。炎症是损伤后组织修复的基本机制,由一系列细胞和微血管反应组成,这些反应旨在清除受损组织并生成新组织。该反应包括微血管通透性升高、循环细胞附着于损伤部位附近的血管、多种细胞类型的迁移、细胞凋亡以及新组织和血管的生长。本综述总结了调节炎症级联反应各要素的主要微血管、细胞和分子机制。分析主要集中于确定主要参与者,特别是信号分子和黏附分子,以及它们在炎症级联反应中的作用方式。我们提出了一个关于血浆中炎症介质产生的新假说,这些炎症介质源自负责消化的胰腺消化酶。炎症级联反应为开发描述人类疾病各个方面的定量模型提供了大量机会。