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Figure 2. Effects of PMN depletion and reconstitution with adoptively transferred PMN on CXCL2/3-induced pain control. Rats were pretreated with i.v. anti-PMN serum (gray bars), control animals received nonimmune rabbit serum (open bars). Two hours after CFA the number of leukocytes in the paw (A) were quantified by flow cytometry. Likewise, paw pressure threshold (PTT) (B) was measured before (baseline) and after intraplantar injection of 100 ng CXCL2/3 (n=6, *P<0.05 t test). C) Different numbers of glycogen-elicited peritoneal PMN from allogenic animals were injected into the inflamed paws of PMN-depleted rats. PPT was obtained 15 min later and again after 100 ng i.p. CXCL2/3 (n=6, * P<0.05, one-way ANOVA, Dunnett method, open bar: before CXCL2/3 without PMN depletion; crosshatched bar: effect of intraplantar CXCL2/3 without PMN depletion, gray bars: PMN depletion, striped bars: PMN reconstitution). D) Effect of ex vivo BAPTA/AM (100 µM) or solvent pretreatment before allogenic PMN transfer. Rats were PMN-depleted and reconstituted as described in (C) using 1 x 106 PMN and CXCL2/3-induced PPT elevation was measured thereafter (n=6, *P<0.05, one-way ANOVA, Student-Newman-Keuls method). Data are expressed as means ± SEM
