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Effect of Atorvastatin on PM10-induced Cytokine Production by Human Alveolar Macrophages and Bronchial Epithelial CellsFrom the University of British Columbia and St. Paul’s Hospital, Vancouver, British Columbia, Canada; Second Department of Internal Medicine, Nagasaki University School of Medicine, Nagasaki, Japan; Environmental Health Directorate, Health Canada, Ottawa, Ontario, Canada; and University of British Columbia and St. Paul’s Hospital, Vancouver, British Columbia, Canada Correspondence: Please address correspondence to Stephan F. van Eeden, James Hogg iCAPTURE Centre for Cardiovascular and Pulmonary Research, St. Paul’s Hospital–University of British Columbia, Room 166, 1081 Burrard Street, St. Paul’s Hospital, Vancouver, British Columbia, Canada V6Z 1Y6.
Exposure to ambient air pollution particles (PM10) has been associated with increased cardiovascular morbidity and mortality. Inhaled pollutants induce a pulmonary and systemic inflammatory response that is thought to exacerbate cardiovascular disease. The 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors (statins) have been shown to have anti-inflammatory effects that could contribute to their beneficial effect in cardiovascular disease. The aim of this study is to determine the effects of statins on PM10-induced cytokine production in human bronchial epithelial cells (HBECs) and alveolar macrophages (AMs). Primary HBECs and AMs are obtained from resected human lung. Cells are pretreated with different concentrations of atorvastatin for 24 hours and then exposed to 100 µg/mL urban air pollution particles (EHC-93). Cytokine levels (interleukin-1β, interleukin-8, granulocyte-macrophage colonystimulating factor, interleukin-6, and tumor necrosis factor-
Key Words: alveolar macrophage • atorvastatin • bronchial epithelial cell • particulate matter
International Journal of Toxicology, Vol. 28, No. 1,
17-23 (2009) |
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) are measured at messenger RNA and protein levels using real-time polymerase chain reaction and bead-based multiplex immunoassay, respectively. PM10 exposure increases production of these cytokines by both cell types. Atorvastatin attenuates PM10-induced messenger RNA expression and cytokine production by AMs but not by HBECs. It is concluded that statins can modulate the PM10-induced inflammatory response in the lung by reducing mediator production by AMs.