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. Author manuscript; available in PMC: 2015 May 1.
Published in final edited form as: J Pain. 2014 May;15(5):496–506. doi: 10.1016/j.jpain.2014.01.491

Figure 4.

Figure 4

Adoptive transfer of WT BMDM prevents and treats persistent IL-1β-induced hyperalgesia in LysM-GRK2+/− mice. (A–D) Thermal sensitivity was assessed over time after intraplantar IL-1β. (A and B) LysM-GRK2+/− mice were injected i.v. with (A) WT BMDM (3.5 − 106 cells per mouse; n = 10), or (B) GRK2+/− BMDM (3.5 − 106 cells per mouse; n = 8 or vehicle (n = 8) 10 minutes before intraplantar IL-1β. (C) WT mice received i.v. WTBMDM(3.5−106 cells per mouse) or vehicle (n = 10 per group) 10 minutes before intraplantar IL-1β. (D) LysM-GRK2+/− received WT or GRK2+/− BMDM (15,000 per mouse) or vehicle i.t. (n = 6 per group) 10 minutes before intraplantar IL-1β. (E) Representative pictures of DRG of LysM-GRK2+/− mice treated with vehicle or WT GFP-BMDM (3.5 − 106 cells per mouse) 10 minutes before intraplantar IL-1β. DRG were isolated 8 hours after intraplantar IL-1β administration and stained for GFP and CD45 to identify transplanted cells. Scale bar indicates 40 μm. (F) WT or GRK2+/− BMDM (3.5 − 106 cells per mouse) or vehicle were administered i.v. 24 hours after intraplantar IL-1β, that is, during already established persistent hyperalgesia in LysM-GRK2+/− mice. Thermal sensitivity was assessed over time (n = 4–8). Data are expressed as mean ± SEM. **P < .01, ***P < .001 WT BMDM vs vehicle. #P < .05, ##P < .01 GRK2+/− BMDM vs vehicle.