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Published ahead of print on August 14, 2003, doi:10.1165/rcmb.2003-0259OC

Am. J. Respir. Cell Mol. Biol., Volume 30, Number 2, February 2004, 202-211

A more recent version of this article appeared on February 1, 2004
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Submitted on July 10, 2003
Revised on August 12, 2003

CIGARETTE SMOKE DECREASES PULMONARY DENDRITIC CELLS AND IMPACTS ANTI-VIRAL IMMUNE RESPONSIVENESS

Clinton S Robbins1, David E Dawe1, Susanna I Goncharova1, Mahmoud A Pouladi1, Anna G Drannik1, Filip K Swirski1, Gerard Cox2, and Martin R Stampfli1*

1 Department of Pathology and Molecular Medicine, Centre for Gene Therapeutics, McMaster University, Hamilton, Ontario, Canada, 2 Department of Medicine, McMaster University, Hamilton, Ontario, Canada

* To whom correspondence should be addressed. E-mail: stampfli{at}mcmaster.ca.

We investigated the impact of cigarette smoke exposure on respiratory immune defense mechanisms. Mice were exposed to two cigarettes daily, five days per week, for 2-4 months. Tobacco smoke decreased the number of dendritic cells (DCs) in the lung tissue. Furthermore, smoke exposure dramatically reduced the percentage of B7.1 expressing DCs. Because DCs are believed to be indispensable to the initiation of adaptive immune responses, we investigated the impact of cigarette smoke on immune responsiveness toward adenovirus. Mice were exposed to two cigarettes for 2-4 months and inoculated with 2x108 pfu of a replication-deficient adenovirus on three occasions, two weeks apart, during the last month of tobacco smoke exposure. Smoke exposure specifically prevented the expansion and maximal activation of CD4 T cells and reduced the number of both activated CD4 and CD8 T cells. Consequently, smoke exposure shifted the activated CD4:CD8 T cell ratio from 3 to 1.5 when compared to sham exposure. Significant decreases were also observed in serum adenovirus-specific panIgG, IgG1 and IgG2a immunoglobulins levels, which was associated with diminished viral neutralization capacity. We demonstrate that chronic tobacco smoke exposure impairs the immune response against adenovirus. This may, in part, explain the increased prevalence of viral infections in COPD.




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