TNFα inhibitor (C87) was used to inhibit TNFα signaling in the presence of oral cancer cell line supernatant. We used the acute cell line supernatant model described in Figure 1 during which mice received 3 consecutive injections of either oral cancer cell line supernatant, HSC3 or SCC9, alone or in a co-injection with C87. Pooled data (B) indicate that C87 alone (C87+DMEM, white square) does not affect gnawing behavior. However, HSC3 (black circle) and SCC9 (gray triangle) containing 0.02% DMSO (HSC3+vehicle and SCC9+vehicle, respectively) evoked a significant increase in gnaw time. Co-administration of C87 with HSC3 (HSC3+C87, white circle, n = 5) or SCC9 (SCC9+C87, white triangle, n = 5) abolished the oral cancer cell line supernatant-induced pain behavior. Flow cytometry on the tongue tissue from these mice was used to measure the inflammatory infiltrate. B) C87+DMEM had no effect on the percent of CD45+ immune cells in the tongue compared to oral cancer cell line supernatant alone (HSC3+veh, SCC9+veh). However, within the Cd45+ immune cell subpopulations (C) there was a significant increase in the neutrophils (Ly6G+) in response to HSC3+C87 co-injection compared to HSC3+vehicle. Co-injection of C87 with either HSC3 or SCC9 also resulted in a significant decrease in T cells (CD3+) compared to HSC3+vehicle or SCC9+vehicle respectively (One-way ANOVA, * p<0.05).