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. 2015 Nov 26;373(22):2183-5.
doi: 10.1056/NEJMcibr1511280.

Resolvin Infectious Inflammation by Targeting the Host Response

Craig R Lee, Darryl C Zeldin

Resolvin Infectious Inflammation by Targeting the Host Response

Craig R Lee et al. N Engl J Med. .
No abstract available

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Figures

Figure 1
Figure 1. Transcellular Biosynthesis and Actions of RvTs
The 13-series resolvins (RvTs) are derived from docosapentaenoic acid (DPA, 22:5, n-3), which is the intermediate metabolite in the fatty acid elongase-2 mediated conversion of eicosapentaenoic acid (EPA 20:5, n-3) to docosahexaenoic acid (DHA, 22:6, n-3). In endothelial cells, cyclooxygenase-2 (COX-2) metabolizes DPA to the intermediate metabolite 13-hydroxydocosapentaenoic acid (13-HDPA), which undergoes transcellular trafficking to adjacent neutrophils and subsequent metabolism by 5-lipoxygenase (5-LOX) to form the four distinct RvT products (RvT1, RvT2, RvT3 and RvT4). Atorvastatin enhances RvT biosynthesis via S-nitrosylation of endothelial COX-2, whereas the COX-2 inhibitor celecoxib suppresses endothelial 13-HDPA biosynthesis. Once formed, RvTs have a myriad of potent autocrine and paracrine effects that promote resolution of infectious inflammation. They promote bacterial phagocytosis in macrophages and neutrophils, and increase production of reactive oxygen species (ROS), block activation of inflammasome components (caspase-1, IL-1β) and attenuate production of pro-inflammatory eicosanoids (LTB4, PGD2, PGE2, TxB2, PGF2α) in macrophages.
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