To date, there has been no study on the effects of interleukin-10 (IL-10) on complex regional pain syndrome (CRPS) rodent models, despite the anti-allodynic effect of IL-10 in previous studies. Thus, the aim of this study was to investigate the effect of IL-10 in a CRPS mouse model and find whether early inhibition of neuro-inflammation by IL-10 administration, which is considered to be one of the important mechanisms in the generation of central sensitization, could prevent the transition from the acute stage to the chronic stage of CRPS.
A mouse model of CRPS (n=6/group) involving tibia fracture/cast immobilization to test the efficacy of intrathecal IL-10 (0.3 μg/5 μL −1 day −1 for 7 days) or vehicle during the acute (3 weeks after fracture) stage of CRPS.
Intrathecal recombinant IL-10 (rIL-10) administration was anti-allodynic in the acute stage of the CRPS mouse model, and these anti-allodynic effects of IL-10 developed by modulating microglial activation and decreasing NK1 receptor expression in the spinal cord. However, intrathecal rIL-10 administration in the acute stage of the CRPS mouse model cannot prevent the transition to the chronic stage of CRPS in the acute stage of CRPS.
Collectively, these results demonstrate that intrathecally administered rIL-10 attenuates mechanical allodynia in the CRPS mouse model. However, this effect of IL-10 on allodynia in the acute stage of CRPS was not sufficient to prevent the transition to the chronic stage of CRPS. In the future, further studies about the mechanisms of central sensitization in CRPS will be necessary.