Accelerating the reversal of inflammatory pain with NPD1 and its receptor GPR37
Lintao Qu, Michael J. Caterina
Lintao Qu, Michael J. Caterina
Published August 1, 2018; First published July 16, 2018
Citation Information: J Clin Invest. 2018;128(8):3246-3249. https://doi.org/10.1172/JCI122203.
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Commentary

Accelerating the reversal of inflammatory pain with NPD1 and its receptor GPR37

Abstract

Resolution of inflammation is a critical process that is facilitated by specialized proresolving mediators (SPMs). In this issue, Bang et al. show that the G protein–coupled receptor GPR37 is a receptor for one such SPM, neuroprotectin D1. They also show that GPR37 activation in macrophages enhances phagocytosis, shifts cytokine release toward an antiinflammatory profile, and thereby helps to reverse inflammatory pain.

Authors

Lintao Qu, Michael J. Caterina

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Figure 1

NPD1-GPR37 signaling promotes resolution of inflammatory pain.

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NPD1-GPR37 signaling promotes resolution of inflammatory pain. (A) Biosy...
(A) Biosynthesis of neuroprotectin D1 (NPD1) from dietary docosahexaenoic acid (DHA). (B) Genetic knockout of the NPD1 receptor GPR37 prolongs pain evoked by zymosan injection without altering kinetics of immune cell trafficking or resolution of edema. (C) NPD1 and GPR37 signaling likely promotes resolution of inflammatory pain by both enhancing macrophage phagocytosis and shifting cytokine release toward an antiinflammatory profile. Onset of inflammation is at left; resolution phase is at right.