[Inflammation, immunity and surgery]
- PMID: 7552389
[Inflammation, immunity and surgery]
Abstract
The activation of endothelial and phagocytic cells, with concomitant formation of a range of adhesive molecules and inflammatory mediators, are integral parts of the host response to injurious agents (trauma, infection, altered antigens, toxins, chemicals etc.). The excessive mediator responses are associated with increased morbidity and lethality. Cytokines, soluble mediators secreted by cells, play an integral role in the metabolic and immune responses to the injurious agents. Widespread tissue damage, when associated with fulminant sepsis may induce massive release of cytokines (TNF, IL-1, IL-6), triggering certain steps of reactions involving multiple organs and culminating in the systemic inflammatory response syndrome, sepsis syndrome or multiple organ failure syndrome. (Fig. 2, Ref. 21.)
Similar articles
-
[Inflammation: biological and clinical features--management].Rev Prat. 2007 Apr 15;57(7):775-80. Rev Prat. 2007. PMID: 17626324 French. No abstract available.
-
Mediators of injury and inflammation.World J Surg. 1996 May;20(4):406-10. doi: 10.1007/s002689900064. World J Surg. 1996. PMID: 8662127 Review.
-
Endothelial cells: role in infection and inflammation.World J Surg. 1998 Feb;22(2):171-8. doi: 10.1007/s002689900366. World J Surg. 1998. PMID: 9451933 Review.
-
Systemic inflammation after trauma.Injury. 2007 Dec;38(12):1336-45. doi: 10.1016/j.injury.2007.10.003. Epub 2007 Nov 28. Injury. 2007. PMID: 18048040 Review.
-
Selective blockade of endothelial NF-kappaB pathway differentially affects systemic inflammation and multiple organ dysfunction and injury in septic mice.J Pathol. 2010 Mar;220(4):490-8. doi: 10.1002/path.2666. J Pathol. 2010. PMID: 20020511