Abstract

Inflammatory macrophages play a fundamental role in neuropathic pain. In this study, we demonstrate the effects of peripheral interleukin-13 (IL-13) on neuropathic pain after partial sciatic nerve (SCN) ligation (PSL) in mice. IL-13 receptor α1 was upregulated in accumulating macrophages in the injured SCN after PSL. Treatment with IL-13 reduced inflammatory macrophage-dominant molecules and increased suppressive macrophage-dominant molecules in cultured lipopolysaccharide-stimulated peritoneal macrophages and ex vivo SCN subjected to PSL. Moreover, the perineural administration of IL-13 relieved tactile allodynia after PSL. These results suggest that IL-13 reverses inflammatory macrophage-dependent neuropathic pain via a phenotype shift toward suppressive macrophages.

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