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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #163994
Title: EMPHYSEMATOUS LUNG DESTRUCTION BY CIGARETTE SMOKE. THE EFFECTS OF LATENT ADENOVIRAL INFECTION ON THE LUNG INFLAMMATORY RESPONSE

Author
item MESHI, BERNARD - UBC MCDONALD RES LAB
item VITALIS, TIMOTHY - UBC MCDONALD RES LAB
item IONECU, DIANA - UBC MCDONALD RES LAB
item ELLIOT, MARK - UBC MCDONALD RES LAB
item LIU, CHUN - TUFTS-HNRCA
item WANG, XIANG-DONG - TUFTS-HNRCA
item HAYASHI, SHIZU - UBC MCDONALD RES LAB
item HOGG, JAMES - UBC MCDONALD RES LAB

Submitted to: American Journal of Respiratory Cell and Molecular Biology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/5/2001
Publication Date: 3/1/2002
Citation: MESHI, B., VITALIS, T.Z., IONECU, D., ELLIOT, M.W., LIU, C., WANG, X., HAYASHI, S., HOGG, J.C. EMPHYSEMATOUS LUNG DESTRUCTION BY CIGARETTE SMOKE. THE EFFECTS OF LATENT ADENOVIRAL INFECTION ON THE LUNG INFLAMMATORY RESPONSE. American Journal of Respiratory Cell and Molecular Biology. 2002;26:52-57.

Interpretive Summary: This study was designed to test the hypothesis that cigarette smoke-induced inflammation and emphysema are amplified by the presence of latent adenoviral (Ad) infection, and to determine whether this emphysematous process can be reversed by all-trans-retinoic acid treatment. The results confirm that in guinea pigs, chronic cigarette-smoke exposure caused lesions similar to human centrilobular emphysema. We also show that latent Ad infection combined with cigarette-smoke exposure caused an excess increase in lung volume, air-space volume, and lung weight, and further decrease in surface-to-volume ratio compared with smoke exposure alone. Retinoic acid treatment failed to reverse these emphysematous changes. We conclude that latent Ad infection amplifies the emphysematous lung destruction and increases the inflammatory response produced by cigarette-smoke exposure.

Technical Abstract: This study was designed to test the hypothesis that cigarette smoke-induced inflammation and emphysema are amplified by the presence of latent adenoviral (Ad) infection, and to determine whether this emphysematous process can be reversed by all-trans-retinoic acid (RA) treatment. The results confirm that in guinea pigs, chronic cigarette-smoke exposure caused lesions similar to human centrilobular emphysema. They also show that latent Ad infection combined with cigarette-smoke exposure caused an excess increase in lung volume (P < 0.001), air-space volume (P < 0.001), and lung weight (P < 0.01), and further decrease in surface-to-volume ratio (P < 0.001) compared with smoke exposure alone. RA treatment failed to reverse these emphysematous changes. Analysis of inflammatory response in parenchymal and airway tissue showed that smoking caused an increase of polymorphonuclear leukocytes (PMNs) (P < 0.0002), macrophages (P < 0.001), and CD4 cells (P < 0.0009), and that latent Ad infection independently increased PMNs (P < 0.001), macrophages (P = 0.003), and CD8 cells (P < 0.001). We conclude that latent Ad infection amplifies the emphysematous lung destruction and increases the inflammatory response produced by cigarette-smoke exposure. In this study, the increase in CD4 was associated with cigarette smoke and the increase in CD8 cells with latent Ad infection.