Lung inflammation was induced by CLP as assessed by increased IL-6, TNF-α, IL-1β, keratinocyte chemoattractant (KC), and macrophage inflammatory protein-2 (MIP-2), as well as MPO activity in the lungs, whereas those parameters were significantly decreased in OP18-treated mice, indicating that OP18 mitigated lung inflammation and neutrophil influx in the septic lungs (Figures 5A–F). The gene discussed is MPO; the disease is inflammatory response.