Recently, we have examined the effect of the endogenous PPAR-γ agonist 15-deoxy-Δ12,14-prostaglandin J2 (15d-PG J2) on acute lung injury induced by LPS in mice.9 We treated ICR mice with 15d-PG J2 (10 μg/kg, 100 μg/kg, or 1 mg/kg) before intratracheal challenge with LPS (125 μg/kg). Unexpectedly, 15d-PG J2, at a dose of 1 mg/kg, did not ameliorate the neutrophilic lung inflammation and pulmonary edema induced by LPS, but, rather, enhanced them. The enhancement was concomitant with the increased lung expression of interleukin-1β, macrophage inflammatory protein-1α, and macrophage chemoattractant protein-1. Interestingly, 15d-PG J2 increased the nuclear protein expression of PPAR-γ and inhibited the nuclear localization of NF-κB related to LPS in murine lungs. In the study, we concluded that 15d-PG J2 may not be useful but may be potentially harmful as a therapeutic option for acute lung injury related to LPS. Therefore, evidence from in vivo studies above the anti-inflammatory effects of statins on sepsis is needed before statins can be used as a therapeutic option in the clinical setting.