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Am J Physiol Cell Physiol 276: C700-C710, 1999;
0363-6143/99 $5.00
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Vol. 276, Issue 3, C700-C710, March 1999

Chemokine expression in CF epithelia: implications for the role of CFTR in RANTES expression

Lisa M. Schwiebert1,2, Kim Estell1, and Stacie M. Propst1

1 Department of Physiology and Biophysics and 2 Gregory Fleming James Cystic Fibrosis Research Center, University of Alabama, Birmingham, Alabama 35294

To delineate the mechanisms that facilitate leukocyte migration into the cystic fibrosis (CF) lung, expression of chemokines, including interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), and RANTES, was compared between CF and non-CF airway epithelia. The findings presented herein demonstrate that, under either basal conditions or tumor necrosis factor-alpha (TNF-alpha )- and/or interferon-gamma (IFN-gamma )-stimulated conditions, a consistent pattern of differences in the secretion of IL-8 and MCP-1 between CF and non-CF epithelial cells was not observed. In contrast, CF epithelial cells expressed no detectable RANTES protein or mRNA under basal conditions or when stimulated with TNF-alpha and/or IFN-gamma (P <=  0.05), unlike their non-CF counterparts. Correction of the CF transmembrane conductance regulator (CFTR) defect in CF airway epithelial cells restored the induction of RANTES protein and mRNA by TNF-alpha in combination with IFN-gamma (P <=  0.05) but had little effect on IL-8 or MCP-1 production compared with mock controls. Transfection studies utilizing RANTES promoter constructs suggested that CFTR activates the RANTES promoter via a nuclear factor-kappa B-mediated pathway. Together, these results suggest that 1) RANTES expression is altered in CF epithelia and 2) epithelial expression of RANTES, but not IL-8 or MCP-1, is dependent on CFTR.

epithelial cells; cystic fibrosis; cystic fibrosis transmembrane conductance regulator; inflammation


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