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Received Jan 20, 2017; Revised Mar 31, 2017; Accepted Apr 20, 2017
This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
1. Introduction
The orchestration of inflammation in response to tissue injury is essential for patient survival. Trauma-associated inflammation is a complex process involving release of danger-associated molecular patterns (DAMP), cell signaling, production and secretion of inflammatory mediators, local regulation of barrier functions, and recruitment of inflammatory cells [1–3]. Recruited leukocytes are essential for the elimination of cellular debris and foreign matter, for the prevention of infections, and for the initiation of tissue regeneration [1–3]. The site of inflammation should, however, communicate with the immune system with utmost caution, as exuberant inflammation carries the risk of inducing systemic inflammatory response syndrome (SIRS) that predisposes to life-threatening complications including systemic barrier dysfunction, sepsis, and multiorgan failure [1–3].
Countless mediators from wounds or other inflammatory sites enter the circulation via damaged blood vessels. The earliest among them is extracellular ATP and chemokines [4, 5]. Extracellular ATP, mainly originating from the cytoplasm of injured cells, is a DAMP that upon binding to receptor P2X7 expressed by primed monocytes/macrophages induces the assembly of the NLRP3 (NACHT,...