Interleukin-1β and interferon-γ differentially regulate release of monocyte chemotactic protein-1 and interleukin-8 by human bronchial epithelial cells

Vincent H J Van Der Velden, Mascha M. Verheggen, Sergio Bernasconi, Silvano Sozzani, Brigitta A E Naber, Carin A J Van Der Linden-van Beurden, Henk C. Hoogsteden, Alberto Mantovani, Marjan Versnel

Research output: Contribution to journalArticle

Abstract

Airway inflammation is characterized by an accumulation of activated leukocytes. Bronchial epithelial cells may contribute to this process by releasing chemokines and by expressing surface membrane molecules involved in the adhesion and activation of the recruited leukocytes. In this study, we analyzed the effects of cytokines and glucocorticoids on the release of monocyte chemotactic protein-1 (MCP-1), a potent chemoattractant for predominantly monocytes and lymphocytes, by human bronchial epithelial cells and compared this with the release of interleukin-8 (IL-8), which potently attracts neutrophils. In addition, we analyzed the effects of cytokines and glucocorticoids on the epithelial expression of intercellular adhesion molecule (ICAM)-1, CD40, and human leukocyte antigen (HLA) class II molecules. Primary cultures of human bronchial epithelial cells constitutively released MCP-1 and IL-8. IFN-γ greatly increased MCP-1 release, which was accompanied by increased expression of MCP-1 mRNA and an increased monocyte chemotactic potential. In contrast, IFN-γ had no effect on the release of IL-8, but it did increase the epithelial expression of ICAM-1, CD40, and HLA class II molecules. IL-1β increased both MCP-1 and IL-8 release, and increased the expression of ICAM-1 and CD40, but not HLA class II molecules. Dexamethasone partially inhibited the cytokine-induced release of MCP-1 and IL-8 and the expression of ICAM-1, CD40, and HLA class II molecules by human bronchial epithelial cells. Our results indicate that IFN-γ and IL-1β differentially regulate the MCP-1 and IL-8 release by human bronchial epithelial cells. In addition, IL-1β and particularly IFN-γ increase the expression of ICAM-1, HLA class II and/or CD40 molecules, which are involved in the adhesion and possibly activation of the recruited leukocytes. Finally, the beneficial effect of glucocorticoid therapy in airway inflammatory diseases may be mediated in part by inhibition of chemokine release and ICAM-1, CD40, and HLA class II expression by bronchial epithelial cells.

Original languageEnglish
Pages (from-to)269-277
Number of pages9
JournalEuropean Cytokine Network
Volume9
Issue number3
Publication statusPublished - 1998

Keywords

  • Bronchial epithelial cells
  • Cytokines
  • Glucocorticoids
  • IL-8
  • MCP-1

ASJC Scopus subject areas

  • Immunology
  • Cell Biology

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  • Cite this

    Van Der Velden, V. H. J., Verheggen, M. M., Bernasconi, S., Sozzani, S., Naber, B. A. E., Van Der Linden-van Beurden, C. A. J., Hoogsteden, H. C., Mantovani, A., & Versnel, M. (1998). Interleukin-1β and interferon-γ differentially regulate release of monocyte chemotactic protein-1 and interleukin-8 by human bronchial epithelial cells. European Cytokine Network, 9(3), 269-277.