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Am J Physiol Lung Cell Mol Physiol 280: L537-L546, 2001;
1040-0605/01 $5.00
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Vol. 280, Issue 3, L537-L546, March 2001

Ozone-induced lung inflammation and hyperreactivity are mediated via tumor necrosis factor-alpha receptors

Hye-Youn Cho, Liu-Yi Zhang, and Steven R. Kleeberger

Department of Environmental Health Sciences, The Johns Hopkins School of Hygiene and Public Health, Baltimore, Maryland 21205

This study was designed to investigate the mechanisms through which tumor necrosis factor (Tnf) modulates ozone (O3)-induced pulmonary injury in susceptible C57BL/6J (B6) mice. B6 [wild-type (wt)] mice and B6 mice with targeted disruption (knockout) of the genes for the p55 TNF receptor [TNFR1(-/-)], the p75 TNF receptor [TNFR2(-/-)], or both receptors [TNFR1/TNFR2(-/-)] were exposed to 0.3 parts/million O3 for 48 h (subacute), and lung responses were determined by bronchoalveolar lavage. All TNFR(-/-) mice had significantly less O3-induced inflammation and epithelial damage but not lung hyperpermeability than wt mice. Compared with air-exposed control mice, O3 elicited upregulation of lung TNFR1 and TNFR2 mRNAs in wt mice and downregulated TNFR1 and TNFR2 mRNAs in TNFR2(-/-) and TNFR1(-/-) mice, respectively. Airway hyperreactivity induced by acute O3 exposure (2 parts/million for 3 h) was diminished in knockout mice compared with that in wt mice, although lung inflammation and permeability remained elevated. Results suggested a critical role for TNFR signaling in subacute O3-induced pulmonary epithelial injury and inflammation and in acute O3-induced airway hyperreactivity.

susceptibility; tumor necrosis factor receptor knockout; pulmonary injury; gene targeting


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