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. 2014 Sep 1;1(3):147-154.
doi: 10.1007/s40472-014-0017-6.

Ischemia/reperfusion Injury and its Consequences on Immunity and Inflammation

Bendix R Slegtenhorst  1 , Frank Jmf Dor  2 , Hector Rodriguez  3 , Floris J Voskuil  4 , Stefan G Tullius  5
Affiliations

Ischemia/reperfusion Injury and its Consequences on Immunity and Inflammation

Bendix R Slegtenhorst et al. Curr Transplant Rep. .

Abstract

Ischemia/reperfusion injury (IRI), an inherent component of transplantation, affects organ quality and transplant outcomes. Although the complexity of the pathophysiology is recognized, detailed mechanisms remain unclear, and strategies preventing the consequences of IRI have been challenging. Of critical significance appears the link between IRI, the initiation of innate immune responses, and the (potential) augmentation of adaptive immunity. An improved understanding of those complex mechanisms and interactions may pave the way for more effective treatment strategies.

Keywords: inflammation; innate immunity; ischemia-reperfusion injury.

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Conflict of interest statement

All authors declare no conflict of interest

Figures

Figure 1
Figure 1
Damage-associated molecular patterns (DAMPs), released from necrotic and injured cells, activate pattern recognition receptors (PRRs) expressed on innate immune cells and epithelial and endothelial cells. Consequently, inflammatory cytokines and chemokines are produced. Injured cells produce reactive oxygen species (ROS) that are cytotoxic. Activated endothelial cells upregulate expression of adhesion molecules, thereby facilitating leukocyte adhesion and transmigration. Neutrophils release neutrophil extracellular traps (NETs) that are both pro-thrombotic and cytotoxic. Neutrophils also engage in the respiratory burst and release their granule proteins. Macrophages and neutrophils release microvesicles containing thrombin and platelets express PRRs that mediate the generation of thrombin. Thrombin activates innate immune cells through proteinase-activated receptor 1 (PAR-1) ligation resulting in the production of inflammatory cytokines and chemokines. The complement system is activated, providing a chemotactic gradient as well as an activating cue for innate immune cells through their cognate receptors.
See this image and copyright information in PMC

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