부산대학교 도서관

Eotaxin, a potent eosinophil-specific chemotactic factor, is increased in the lower respiratory tract of asthma patients. Recently, lung fibroblasts have been reported to produce eotaxin and their activation can be modulated by inflammatory cytokines. To test the hypothesis that inflammatory cytokines modulate the eotaxin release from lung fibroblasts, we investigated the potential of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), or interferon-γ (IFN-γ) to induce the release of eotaxin and eotaxin mRNA by the human fetal lung fibroblast cell line, HFL-1, was evaluated. HFL-1 released eotaxin constitutively without stimulation, but IL-1β or TNF-α stimulated eotaxin release in a dose- and time-dependent manner. IL-1β or TNF-α treatment of HFL-1 also resulted in the augmented expression of eotaxin mRNA. Although IFN-γ alone had negligible effect on eotaxin release and mRNA expression, IFN-γ induced a significant, concentration-dependent attenuation of eotaxin release and eotaxin mRNA expression from HFL1 stimulated with IL-1β or TNF-α . These findings are consistent with the concept that lung fibroblast-derived eotaxin may in part be responsible for the eosinophil infiltration observed in the airways ofasthmatic patients and that network ofcytokines may modulate the eosinophil recruitment to the airways by stimulation of fibroblasts to release eotaxin. [ABSTRACT FROM AUTHOR]