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(American Journal of Pathology. 2006;169:12-20.)
© 2006 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2006.051042

Regulation of Chemokine Expression by NaCl Occurs Independently of Cystic Fibrosis Transmembrane Conductance Regulator in Macrophages

Amanda G. Kostyk*, Karen M. Dahl{dagger}, Murry W. Wynes*{ddagger}, Laurie A. Whittaker§, Daniel J. Weiss§, Roberto Loi§ and David W.H. Riches*{ddagger}

From the Department of Immunology* and the Division of Pulmonary Sciences and Critical Care Medicine, the Department of Medicine, University of Colorado Health Sciences Center, Denver, Colorado; the Division of Infectious Diseases,{dagger} The Children’s Hospital, Denver, Colorado; the Program in Cell Biology,{ddagger} the Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado; and the Division of Pulmonary Critical Care,§ the Department of Medicine, University of Vermont, Burlington, Vermont

Chronic pulmonary inflammation and infection are the leading causes of morbidity and mortality in cystic fibrosis (CF). While the effect of mutation of the cystic fibrosis transmembrane conductance regulator (CFTR) on airways remains controversial, some groups have demonstrated increases in Na+ and Cl– in CF airway surface liquid compared to normal airways. We investigated the consequences of NaCl on pro-inflammatory chemokine and cytokine production by macrophages. Stimulation of mouse macrophages with increasing amounts of NaCl induced macrophage inflammatory protein-2 (MIP-2) and tumor necrosis factor-{alpha} (TNF-{alpha}) production. Further, co-incubation of macrophages with NaCl in the presence of either lipopolysaccharide (LPS) or TNF-{alpha} synergistically increased MIP-2 production. Both the NaCl and NaCl plus LPS responses were partially dependent on endogenous production and autocrine signaling by TNF-{alpha}. To investigate the role of CFTR in MIP-2 production, we compared the responses of wild-type and {Delta}F508 CF mouse macrophages to NaCl and LPS. The responses of macrophages from both strains were indistinguishable. In addition, CFTR mRNA was not expressed in macrophages. Taken together, these findings suggest that NaCl stimulates MIP-2 production by macrophages through a mechanism that is partially dependent on TNF-{alpha} but independent of macrophage CFTR expression.




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