Inflammatory host responses in sepsis.
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.
Zimmerman
J J
JJ
Department of Pediatrics, University of Wisconsin-Madison Medical School.
Ringer
T V
TV
D001685:Biological Factors / Q000096:biosynthesis*; D015815:Cell Adhesion Molecules / Q000096:biosynthesis; D002648:Child; D003167:Complement Activation; D015777:Eicosanoids / Q000096:biosynthesis; D004723:Endorphins / Q000502:physiology; D006801:Humans; D007378:Interleukins / Q000096:biosynthesis; D007962:Leukocytes / Q000276:immunology* / Q000378:metabolism; D015289:Leukotrienes / Q000096:biosynthesis; D010972:Platelet Activating Factor / Q000096:biosynthesis; D018805:Sepsis / Q000276:immunology / Q000503:physiopathology*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis
D001685:Biological Factors; D015815:Cell Adhesion Molecules; D015777:Eicosanoids; D004723:Endorphins; D007378:Interleukins; D015289:Leukotrienes; D010972:Platelet Activating Factor; D014409:Tumor Necrosis Factor-alpha