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J. Biol. Chem., Vol. 278, Issue 50, 50615-50623, December 12, 2003

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Tumor Necrosis Factor Modulates Airway Smooth Muscle Function via the Autocrine Action of Interferon ^*

Omar Tliba, Samira Tliba, Chien Da Huang, Rebecca K. Hoffman, Peter DeLong, Reynold A. Panettieri, Jr., and Yassine Amrani

From the Pulmonary, Allergy and Critical Care Division, Department of Medicine, University of Pennsylvania Medical Center, Philadelphia, Pennsylvania 19104

Current evidence suggests that tumor necrosis factor (TNF) and the family of interferons (IFNs) synergistically regulate many cellular responses that are believed to be critical in chronic inflammatory diseases, although the underlying mechanisms of such interaction are complex, cell-specific, and not completely understood. In this study, TNF in a time-dependent manner activated both janus tyrosine kinase 1 and Tyk2 tyrosine kinase and increased the nuclear translocation of interferon-regulatory factor-1, STAT1, and STAT2 in human airway smooth muscle cells. In cells transfected with a luciferase reporter, TNF stimulated -activated site-dependent gene transcription in a time- and concentration-dependent manner. Using neutralizing antibodies to IFN and TNF receptor 1, we show that TNF-induced secretion of IFN mediated -activated site-dependent gene expression via activation of TNF receptor 1. In addition, neutralizing antibody to IFN also completely abrogated the activation of interferon stimulation response element-dependent gene transcription induced by TNF. Secreted IFN acted as a negative regulator of TNF-induced interleukin-6 expression, while IFN augmented TNF-induced RANTES (regulated on activation normal T cell expressed and secreted) secretion but had little effect on TNF-induced intercellular adhesion molecule-1 expression. Furthermore TNF, a modest airway smooth muscle mitogen, markedly induced DNA synthesis when cells were treated with neutralizing anti-IFN. Together these data show that TNF, via the autocrine action of IFN, differentially regulates the expression of proinflammatory genes and DNA synthesis.

Received for publication, April 9, 2003 , and in revised form, August 18, 2003.

^* This work was supported by National Institutes of Health Grants 2R01-HL55301 (to R. A. P.) and 1P50-HL67663 (to R. A. P.) and by American Lung Association Grant RG-062-N (to Y. A.). 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.

A Parker B. Francis fellow in pulmonary research. To whom correspondence should be addressed: Pulmonary, Allergy and Critical Care Division, University of Pennsylvania Medical Center, 421 Curie Blvd., 848 BRB II/III, Philadelphia, PA 19104-6160. Tel.: 215-573-9851; Fax: 215-573-4469; E-mail: amrani{at}mail.med.upenn.edu.

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