It has been established that the development of COPD is associated with an inflammatory process in the peripheral airways, including the accumulation of neutrophils, macrophages, and lymphocytes.1The activation of neutrophils, producing proteases and oxygen-derived free radicals, is thought to be important in the pathogenesis of the disease, whereas the role of lymphocytes, particularly CD8 cells, remains more controversial.2An important step in the recruitment of leukocytes is the local generation of chemoattractant signals, which mediate the trapping and adhesion on the microvascular endothelium followed by the migration of the cells to the tissue. Interleukin-8 and leukotriene B4 (LTB4) have been identified as important neutrophil chemoattractants in COPD patients.3–4 In particular, LTB4 seems to be the prominent chemotactic factor in patients with the most severe COPD5and during acute exacerbations.6–7 In addition, studies8 have indicated that LTB4 is important for the recruitment of CD8 T cells to sites of inflammation. Whereas the infiltration of CD8 cells was demonstrated in several lung compartments of COPD patients,1,9–10 the evidence of increased numbers of neutrophils in bronchial biopsy specimens and peripheral lung samples from COPD patients is often inconsistent.9–12 The present study focuses on the receptors that mediate LTB4 activity, peroxisome proliferator-activated receptor (PPAR)-α and BLT1. Proinflammatory LTB4 activities are mediated by binding to the BLT1 receptor, which is a high-affinity, G protein-coupled cell surface receptor of LTB4, expressed predominantly in leukocytes.13LTB4 is inactivated through metabolic degradation by the microsomal ω-oxidation and peroxisomal β-oxidation pathways. LTB4 has been reported14to bind and activate PPARα, resulting in the transcription of genes that promote fatty acid degradation. PPARs are a group of transcription factors that regulate the gene expression of enzymes that are associated with lipid homeostasis. Three PPAR subtypes have been identified (α, β/δ, and γ).15Recent evidence has indicated a role for PPARs in the control of various types of inflammatory responses. Most of the antiinflammatory properties of the PPARs arise through their ability to antagonize the nuclear factor (NF)-κB and AP1 signaling pathways.16 It is well-established that the susceptibility of smokers to the development of COPD is associated with an exaggerated inflammatory response in the lungs to cigarette smoke.2 A different ability to mount an inflammatory response, due to diversity in the genes controlling inflammation, may explain the individual differences in the response to smoke, which lead to the characteristic pathologic lesions of COPD in some smokers.