Figure 4.

G protein-coupled CCR3 receptor activation by endogenous CCL5 mediates leptin-induced lipid body-driven LTC₄ synthesis. In (A) human eosinophils were pretreated with pertussis toxin (PTX; 100 ng/mL). In (B) human eosinophils were pretreated with neutralizing anti-CCR3 or anti-CCL5 antibodies (both at 10 μg/mL) or with the PAF receptor antagonist BN52021 (10 μM). All pretreatments were added 30 min before stimulation with hr leptin (50 nM) for 1 h. Lipid body biogenesis was evaluated in osmium-stained cells and LTC₄ production in cell-free supernatants by EIA kits. Values are expressed as the mean ± SEM of at least three distinct donors. + p < 0.05 compared with non-stimulated cells. ^*p < 0.05 compared with leptin-stimulated eosinophils.