Activation of inflammatory responses regulates the transmission of pain pathways through an integrated network in the peripheral and central nervous systems. The immunopotentiator thymosin alpha-1 (Ta1) has recently been reported to have anti-inflammatory and neuroprotective functions in rodents. However, how Ta1 affects inflammatory pain remains unclear. In the present study, intraperitoneal injection of Ta1 attenuated complete Freund's adjuvant (CFA)-induced pain hypersensitivity, and decreased the up-regulation of pro-inflammatory cytokines (TNF-a, IL-1b, and IL-6) in inflamed skin and the spinal cord. We found that CFA-induced peripheral inflammation evoked strong microglial activation, but the effect was reversed by Ta1. Notably, Ta1 reversed the CFA-induced up-regulation of vesicular glutamate transporter (VGLUT) and down-regulated the vesicular c-aminobutyric acid transporter (VGAT) in the spinal cord. Taken together, these results suggest that Ta1 plays a therapeutic role in inflammatory pain and in the modulation of microgliainduced pro-inflammatory cytokine production in addition to mediation of VGLUT and VGAT expression in the spinal cord.Keywords Thymosin alpha-1 Á Cytokine Á Microglia Á Vesicular glutamate transporter type 2 Á Vesicular caminobutyric acid transporter
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