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Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Resolution of sickle cell disease-associated inflammation and tissue damage with 17 R -resolvin D1.
Blood 2019 January 18
Resolvins (Rvs), endogenous lipid mediators, play a key role in the resolution of inflammation. Sickle cell disease (SCD), a genetic disorder of hemoglobin, is characterized by inflammatory and vaso-occlusive pathologies. We document altered proresolving events following hypoxia/reperfusion in humanized SCD mice. We demonstrate novel protective actions of 17 R -resolvin D1 (17 R- RvD1; 7 S , 8 R , 17 R -trihydroxy-4 Z , 9 E , 11 E , 13 Z , 15 E , 19 Z -docosahexaenoic acid) in reducing ex vivo human SCD blood leukocyte recruitment by microvascular endothelial cells and in vivo neutrophil adhesion and transmigration. In SCD mice exposed to hypoxia/reoxygenation, oral administration of 17 R - RvD1 reduces systemic/local inflammation and vascular dysfunction in lung and kidney. The mechanism of action of 17 R -RvD1 involves (1) enhancement of SCD erythrocytes and polymorphonuclear leukocyte efferocytosis, (2) blunting of NF-κB activation, and (3) a reduction in inflammatory cytokines, vascular activation markers, and E-selectin expression. Thus, 17 R -RvD1 might represent a new therapeutic strategy for the inflammatory vasculopathy of SCD.
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