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.

中文翻译：

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分析炎症。

过去，炎症与感染和免疫系统有关。但是，最近的证据表明，范围更广的疾病具有明显的炎症标志物。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，这些反应可用于清除受损组织并生成新组织。级联反应包括微血管的通透性升高，循环细胞附着在损伤部位附近的血管，几种细胞类型的迁移，细胞凋亡以及新组织和血管的生长。这篇综述总结了调节炎症级联反应的主要微血管，细胞和分子机制。分析主要集中在主要参与者的识别上，特别是信号传导和粘附分子及其在炎症级联反应中的作用方式。我们提出了一个新的假设，认为血浆中炎症介质的产生是由负责消化的消化胰酶产生的。炎症级联为描述人类疾病各个方面的定量模型的开发提供了大量机会。