Sepsis-induced inhibition of PMN chemotaxis is reversed by blocking activation of PPAR-γ, expression of which is increased in sepsis. (A left) Peripheral blood PMNs were isolated from control subjects (healthy volunteers [n = 7] and nonseptic patients in the intensive care unit [n = 3]) and patients with sepsis (n = 14). Relative expression of PPAR-γ was plotted as the fold change from healthy controls. PPAR-γ mRNA levels at specific time points after induction of sepsis by (center) LPS administration (1 mg/kg) or by (right) CLP were plotted as the fold change compared with PMNs from vehicle-treated or sham-operated (control) mice, arbitrarily assigned a value of 1. In all panels, β-actin measurements were used for normalization. *P < .05 compared with each control group. (B) Blood PMNs were isolated from mice (n = 8 mice/group) that were rendered septic by intraperitoneal administration of LPS (1 mg/kg) 6 hours previously. Some mice also received GW9662 (1 mg/kg; GW) or vehicle (Veh) by intraperitoneal injection 30 minutes after LPS. Chemotactic responses to leukotriene B₄ (10⁻⁷ M) were measured and are reported as the number of cells per high-power field. *P < .05 compared with control (Veh). (C) Mice (n = 4/group) underwent CLP (■) or sham operation (□). Some mice also received GW9662 (1 mg/kg; GW) or vehicle (Veh) intraperitoneally 30 minutes after the operation. Six hours later animals were killed, and the number of PMNs in the peritoneal cavity was determined as described in “Methods.” *P < .05 compared with control (Veh). Error bars represent SEM.