Zimmerman J J, Ringer T V
Department of Pediatrics, University of Wisconsin-Madison Medical School.
Crit Care Clin. 1992 Jan;8(1):163-89.
Although microbes and their associated toxins initiate sepsis, it is the subsequent host inflammatory response that defines most of what we characterize as clinical sepsis. This article considers the various cellular as well as humoral mediators involved in this response in addition to the complex networking that may result in both augmentation and modulation of the inflammatory response in sepsis.
尽管微生物及其相关毒素引发脓毒症，但随后的宿主炎症反应才定义了我们所描述的大多数临床脓毒症特征。本文除了考虑参与该反应的各种细胞和体液介质外，还探讨了可能导致脓毒症炎症反应增强和调节的复杂网络。
