Shanley T P, Warner R L, Ward P A
University of Michigan Medical School, Department of Pathology, Ann Arbor.
Mol Med Today. 1995 Apr;1(1):40-5. doi: 10.1016/1357-4310(95)80019-0.
Clinicians are constantly challenged by patients who demonstrate the ill effects of an uncontrolled host inflammatory response. Patients with sepsis and adult respiratory distress syndrome (ARDS) are frequently encountered examples of this syndrome. Despite advances in intensive care, mortality from these syndromes remains unchanged over the past two decades. In order to gain a better understanding of this pathophysiological response and to identify more specific therapeutic targets, the techniques of molecular biology have been applied to in vivo inflammatory models. Recent data indicate that the inflammatory response is dependent on the presence of both cytokines and adhesion molecules that mediate neutrophil-endothelial cell adhesive interactions. In this article, we review our experience using a lung model of inflammation that has provided insight into the events leading to injury. Cytokines [particularly, interleukin 1 (IL-1) and tumor necrosis factor alpha (TNF-alpha)], and endothelial, as well as leukocyte, adhesion molecules appear to coordinate a cascade of interactions between leukocytes and endothelial cells, which results in tissue injury.
患者表现出失控的宿主炎症反应所带来的不良影响。脓毒症和成人呼吸窘迫综合征（ARDS）患者就是该综合征常见的例子。尽管重症监护取得了进展，但在过去二十年中，这些综合征导致的死亡率仍未改变。为了更好地理解这种病理生理反应并确定更具体的治疗靶点，分子生物学技术已被应用于体内炎症模型。最近的数据表明，炎症反应依赖于细胞因子和介导中性粒细胞与内皮细胞黏附相互作用的黏附分子的存在。在本文中，我们回顾了我们使用肺部炎症模型的经验，该模型为导致损伤的事件提供了深入了解。细胞因子[特别是白细胞介素1（IL-1）和肿瘤坏死因子α（TNF-α）]以及内皮细胞和白细胞黏附分子似乎协调了白细胞与内皮细胞之间的一系列相互作用，从而导致组织损伤。
