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Acrolein Inhalation Suppresses Lipopolysaccharide-Induced Inflammatory Cytokine Production but Does Not Affect Acute Airways Neutrophilia¹

David Itiro Kasahara^*, Matthew E. Poynter, Ziryan Othman^*, David Hemenway and Albert van der Vliet^2,*

^* Department of Pathology and Department of Medicine, Vermont Lung Center, College of Medicine, and Department of Civil Engineering, University of Vermont, Burlington, VT 05405

Acrolein is a reactive unsaturated aldehyde that is produced during endogenous oxidative processes and is a major bioactive component of environmental pollutants such as cigarette smoke. Because in vitro studies demonstrate that acrolein can inhibit neutrophil apoptosis, we evaluated the effects of in vivo acrolein exposure on acute lung inflammation induced by LPS. Male C57BL/6J mice received 300 µg/kg intratracheal LPS and were exposed to acrolein (5 parts per million, 6 h/day), either before or after LPS challenge. Exposure to acrolein either before or after LPS challenge did not significantly affect the overall extent of LPS-induced lung inflammation, or the duration of the inflammatory response, as observed from recovered lung lavage leukocytes and histology. However, exposure to acrolein after LPS instillation markedly diminished the LPS-induced production of several inflammatory cytokines, specifically TNF-, IL-12, and the Th1 cytokine IFN-, which was associated with reduction in NF-B activation. Our data demonstrate that acrolein exposure suppresses LPS-induced Th1 cytokine responses without affecting acute neutrophilia. Disruption of cytokine signaling by acrolein may represent a mechanism by which smoking contributes to chronic disease in chronic obstructive pulmonary disease and asthma.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grants R01 HL068865 and HL074295.

² Address correspondence and reprint requests to Dr. Albert van der Vliet, Department of Pathology, College of Medicine, University of Vermont, 89 Beaumont Avenue, Burlington VT 05405. E-mail address: albert.van-der-vliet{at}uvm.edu

³ Abbreviations used in this paper: ppm, parts per million; GSH, glutathione; i.t., intratracheal.

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