Pathophysiology of the systemic inflammatory response after major accidental trauma

Table 1 Mediators of the inflammatory response following trauma

	Secretion stimulated by	Cellular origin	Function	Ref.
IL-1(β)	Activation of macrophages	Released from monocytes and endothelium	Pro-inflammatory Induces fever, secretion of IL-6 and 8	[23]
IL-4	Trauma	Activated T-cells	Anti-inflammatory	[45]
IL-6	IL-1β TNF-α	Released from monocytes and endothelium	Pro- and Anti-inflammatory, production of CRP, procalcitonin. IL1R-antagonist, PGE2	[22, 26]
IL-8	IL-1 (β)	Released from monocytes and endothelium	Pro-inflammatory, activate PMN, attracts monocytes, fibroblasts. Prolongs half-life of PMN	[24]
IL-10	PGE2	Released from monocytes and endothelium	Anti-inflammatory	[25]
TNF-α	Activation of macrophages	Monocytes and endothelium	Induces secretion of IL-6 and 8	[22]
IFN-γ	Trauma	NK- cells Activated T-cells	Pro-inflammatory	[42]
HMGB1	Always localized in the nucleus of the cells	Released from nucleus of necrotic cells	Attracts neutrophils and macrophages	[17]
MPO	Activated PMN	Released from granules in monocytes and PMN	Degrades bacteria and cellular debris	[36, 37]
Elastase	Activated PMN	Released from granules in monocytes and PMN	Degrades bacteria and cellular debris	[36, 37]
Free oxygen radicals	Activated PMN	Released from monocytes and PMN	Degrades bacteria and cellular debris	[36, 37]

ISSN: 1757-7241