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Original Research: COPD |

Up-Regulated Membrane and Nuclear Leukotriene B4 Receptors in COPD*

Emanuela Marian, PhD; Simonetta Baraldo, PhD; Annalisa Visentin, MD; Alberto Papi, MD; Marina Saetta, MD; Leonardo M. Fabbri, MD, FCCP; Piero Maestrelli, MD
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*From the Departments of Environmental Medicine and Public Health (Drs. Marian, Visentin, and Maestrelli), and Cardiothoracic and Vascularis Sciences (Drs. Baraldo and Saetta), University of Padova, Padova, Italy; the Department of Clinical and Experimental Medicine (Dr. Papi), University of Ferrara, Ferrara, Italy; and the Department of Medical, Oncological and Radiological Sciences (Dr. Fabbri), University of Modena, Modena, Italy.

Correspondence to: Piero Maestrelli, MD, Dipartimento di Medicina Ambientale e Sanità Pubblica, Università degli Studi di Padova, via Giustiniani, 2, 35128 Padova, Italy; e-mail: piero.maestrelli@unipd.it



Chest. 2006;129(6):1523-1530. doi:10.1378/chest.129.6.1523
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Study objectives: We investigated the role of two leukotriene B4 (LTB4) receptors, BLT1 and peroxisome proliferator-activated receptor (PPAR)-α, in conferring the susceptibility to develop COPD in smokers. Proinflammatory LTB4 activities are mediated by BLT1, while the inactivation of LTB4 is promoted by PPARα.

Patients and methods: BLT1 and PPARα proteins were quantified by immunohistochemistry in specimens obtained during lung surgery from 19 smokers with or without COPD and from 7 nonsmoking subjects.

Results: We have shown that the percentages of PPARα-positive alveolar macrophages and PPARα-positive cells in the alveolar wall were increased in COPD patients compared with control subjects. Moreover, the patients with COPD exhibited a significant increase of BLT1-positive alveolar macrophages compared with nonsmokers and an increased number of BLT1-positive cells in the alveolar walls compared with non-COPD smokers. In contrast, BLT1 and PPARα immunoreactivity did not differ significantly between nonsmokers and non-COPD smokers. Most of BLT1-positive cells in the alveolar walls were neutrophils and CD8 cells. While the number of neutrophils infiltrating the lung parenchyma was similar among the three groups, the number of CD8 T cells was increased in COPD patients, but there was no evidence that BLT1 was up-regulated specifically on these cells in COPD patients.

Conclusion: The results demonstrated that BLT1 and PPARα are detectable in alveolar macrophages and CD8 T cells in human lung tissue, and suggest that the dual LTB4 receptor system is up-regulated in the peripheral lungs of smokers who are susceptible to the development of COPD. This system might represent a novel target for therapeutic intervention in COPD patients.

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