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Published on: September 7, 2019
Spinal macrophage migration inhibitory factor contributes to the pathogenesis of inflammatory hyperalgesia in rats
FuZhou Wang1, XiaoFeng Shen, XiRong Guo
1State Key Laboratory of Pharmaceutical Biotechnology, School of Life Science, Nanjing University, No. 22, Hankou Road, Nanjing 210093, Jiangsu, China Department of Anesthesiology, The Affiliated Nanjing Maternity and Child Health Care Hospital, Nanjing Medical University, Nanjing 210004, Jiangsu, China The Institute of Pediatrics, The Affiliated Nanjing Maternity and Child Health Care Hospital, Nanjing Medical University, Nanjing 210004, Jiangsu, China.
Abstract:
Pro-inflammatory cytokine production after nociceptive stimuli is pivotal for hyperalgesia. As macrophage migration inhibitory factor (MIF), a pleiotropic cytokine produced mainly by nonneuronal tissue, has been involved in the regulation of neuronal functions, herein we examined the role for MIF in formalin-induced inflammatory pain model. MIF critically contributed to nociceptive behaviors following formalin injection. Specifically, spinal administration of a MIF inhibitor (ISO-1) prevented and reversed flinching responses in rats. Further examination showed that levels of both MIF and the MIF receptor CD74 were substantially increased within the ipsilateral spinal cord dorsal horn after formalin administration. Mechanistic studies revealed that MIF upregulated the expression of the spinal NMDA receptor subunit NR2B via the MAPK signaling pathway. Moreover, microglial cells were found to be the major source of spinal MIF after formalin administration by fluorescence colocalization. These data highlight spinal MIF plays a critical role in the pathogenesis of formalin-induced inflammatory pain and suggest MIF may be a potential target for therapy of such pathological condition.