Am. J. Respir. Cell Mol. Biol., Volume 26, Number 5, May, 2002 594-601

Interferon- Enhances Rhinovirus-Induced RANTES Secretion by Airway Epithelial Cells

Shinichi Konno, Kristine A. Grindle, Wai-Ming Lee, Mary K. Schroth, Anne G. Mosser, Rebecca A. Brockman-Schneider, William W. Busse, and James E. Gern

Departments of Medicine, Pediatrics, and Molecular Virology, University of Wisconsin-Madison, Madison, Wisconsin

Respiratory viruses, including rhinoviruses, infect respiratory epithelium and induce a variety of cytokines and chemokines that can initiate an inflammatory response. Cytokines, such as interferon (IFN)- and tumor necrosis factor (TNF)-, could enhance epithelial cell activation by inducing virus receptors. To test this hypothesis, effects of IFN- or TNF- on expression of intercellular adhesion molecule (ICAM)-1, rhinovirus binding, and virus-induced chemokine secretion on A549 and human bronchial epithelial cells (HBEC) were determined. The results varied with the type of cell. IFN- was a stronger inducer of ICAM-1 and viral binding on HBEC, whereas TNF- had greater effects on A549 cells. In addition, IFN-, but not TNF-, synergistically enhanced regulated on activation, normal T cells expressed and secreted (RANTES) mRNA expression and protein secretion induced by RV16 or RV49. To determine whether IFN- could enhance RANTES secretion independent of effects on ICAM-1 and RV binding, HBEC were transfected with RV16 RNA in the presence or absence of IFN-. RV16 RNA alone stimulated RANTES secretion, and this effect was enhanced by IFN-. These results demonstrate that IFN- can enhance rhinovirus-induced RANTES secretion by increasing viral binding, and through a second receptor-independent pathway. These findings suggest that IFN-, by upregulating RANTES secretion, could be an important regulator of the initial immune response to rhinovirus infections.

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