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Am J Physiol Lung Cell Mol Physiol 281: L1288-L1302, 2001;
1040-0605/01 $5.00
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Vol. 281, Issue 5, L1288-L1302, November 2001

IL-4 differentially regulates eotaxin and MCP-4 in lung epithelium and circulating mononuclear cells

Hidetoshi Nakamura1, Andrew D. Luster2, Hiroki Tateno3, Sean Jedrzkiewicz1, Gen Tamura1, Kathleen J. Haley1, Eduardo A. Garcia-Zepeda2, Kazuhiro Yamaguchi3, and Craig M. Lilly1

1 Combined Program in Pulmonary and Critical Care Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston 02115; 2 Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, and Harvard Medical School, Charlestown, Massachusetts 02129; and 3 Department of Medicine, School of Medicine, Keio University, Tokyo 160, Japan

To investigate the mechanisms of eosinophil recruitment in allergic airway inflammation, we examined the effects of interleukin (IL)-4, a Th2-type cytokine, on eotaxin and monocyte chemoattractant protein-4 (MCP-4) expression in human peripheral blood mononuclear cells (PBMCs; n = 10), in human lower airway mononuclear cells (n = 5), in the human lung epithelial cell lines A549 and BEAS-2B, and in human cultured airway epithelial cells. IL-4 inhibited eotaxin and MCP-4 mRNA expression induced by IL-1beta and tumor necrosis factor-alpha in PBMCs but did not significantly inhibit expression in epithelial cells. Eotaxin and MCP-4 mRNA expression was not significantly induced by proinflammatory cytokines in lower airway mononuclear cells. IL-1beta -induced eotaxin and MCP-4 protein production was also inhibited by IL-4 in PBMCs, whereas IL-4 enhanced eotaxin protein production in A549 cells. In contrast, dexamethasone inhibited eotaxin and MCP-4 expression in both PBMCs and epithelial cells. The divergent effects of IL-4 on eotaxin and MCP-4 expression between PBMCs and epithelial cells may create chemokine concentration gradients between the subepithelial layer and the capillary spaces that may promote the recruitment of eosinophils to the airway in Th2-type responses.

interferon-gamma ; interleukin-8; A549 cells; BEAS-2B cells; peripheral blood mononuclear cells; interleukin-4; monocyte chemoattractant protein-4


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