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American Journal of Respiratory and Critical Care Medicine Vol 166. pp. 849-854, (2002)
© 2002 American Thoracic Society

Original Articles

Tumor Necrosis Factor-{alpha} Is Central to Acute Cigarette Smoke–induced Inflammation and Connective Tissue Breakdown

Andrew Churg, Jin Dai, Hsin Tai, Changshi Xie and Joanne L. Wright

Department of Pathology, University of British Columbia, Vancouver, British Columbia, Canada

Correspondence and requests for reprints should be addressed to Andrew Churg, M.D., Department of Pathology, University of British Columbia, 2211 Wesbrook Mall, Vancouver, BC, Canada V6T 2B5. E-mail: achurg{at}interchange.ubc.ca

The role of tumor necrosis factor-{alpha} (TNF-{alpha}) as a mediator of cigarette smoke–induced disease is controversial. We exposed mice with knocked-out p55/p75 TNF-{alpha} receptors (TNF-{alpha}–RKO mice) to cigarette smoke and compared them with control mice. Two hours after smoke exposure, increases in gene expression of TNF-{alpha}, neutrophil chemoattractant, macrophage inflammatory protein-2, and macrophage chemoattractant, protein-1 were seen in control mice. By 6 hours, TNF-{alpha}, macrophage inflammatory protein-2, and macrophage chemoattractant protein-1 gene expression levels had returned to control values in control mice and stayed at control values through 24 hours. In TNF-{alpha}–RKO mice, no changes in gene expression of these mediators were seen at any time. At 24 hours, control mice demonstrated increases in lavage neutrophils, macrophages, desmosine (a measure of elastin breakdown), and hydroxyproline (a measure of collagen breakdown), whereas TNF-{alpha}–RKO mice did not. In separate experiments, pure strain 129 mice, which produce low levels of TNF-{alpha}, showed no inflammatory response to smoke at 24 hours or 7 days. We conclude that TNF-{alpha} is central to acute smoke-induced inflammation and resulting connective tissue breakdown, the precursor of emphysema. The findings support the idea that TNF-{alpha} promoter polymorphisms may be of importance in determining who develops smoke-induced chronic obstructive pulmonary disease.

Key Words: COPD • macrophage inflammatory protein-2 • macrophage chemoattractant protein-1 • polymorphisms • TNF-{alpha}




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