Selective induction of intercellular adhesion molecule-1 by interferon-γ in human airway epithelial cells

D. C. Look, S. R. Rapp, B. T. Keller, M. J. Holtzman

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152 Scopus citations

Abstract

To evaluate the factors controlling migration of leukocytes into pulmonary airway epithelium, we determined the biochemical mechanisms responsible for the regulation of intercellular adhesion molecule-1 (ICAM-1) expression on cultured monolayers of human tracheal epithelial cells (HTECs) or SV40 virus- transformed human bronchial epithelial cells (BEAS-2B). Validation experiments with human umbilical vein endothelial cells (HUVECs) demonstrated little detectable ICAM-1 expression on unstimulated cells or on cells incubated with interferon-γ (IFN-γ), but HUVEC monolayers responded to interleukin-1β (IL-1β) or tumor necrosis factor-α (TNF-α) with significant increases in ICAM-1 and ICAM-1-dependent adherence of polymorphonuclear leukocytes (PMNs). HTEC monolayers also exhibited no significant basal ICAM-1 expression but, in contrast to HUVEC monolayers, had marked increases in ICAM-1 expression and ICAM-1-dependent PMN adherence only after incubation with IFN-γ (and not after IL-1β or TNF-α) treatment. BEAS-2B cells also exhibited relatively selective IFN-γ stimulation of ICAM- 1 expression and ICAM-1-dependent PMN adherence but (like late passage HTEC) showed significant basal ICAM-1 expression. Differences in IFN-γ effect on ICAM-1 levels between HUVEC and HTEC monolayers were not due to differences in number or responsiveness of IFN-γ receptors, because both cell types exhibited a similar number of receptors and other IFN-γ-dependent responses of HUVECs remained active. In all analyses, ICAM-1 mRNA levels correlated closely with detection of ICAM-1 on the cell surface. The results indicate that ICAM-1 is expressed on human airway epithelial cells and that ICAM-1- dependent mechanisms may mediate PMN adherence to these cells. As in other cell types, induction of ICAM-1 in airway epithelial cells appears to be transcriptionally regulated, but in contrast to endothelial cells, the induction of ICAM-1 in airway epithelial cells is selectively responsive to IFN-γ.

Original languageEnglish
Pages (from-to)L79-L87
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume263
Issue number1 7-1
StatePublished - Jan 1 1992

Keywords

  • inflammation
  • interleukin-1β
  • polymorphonuclear leukocyte adherence
  • tumor necrosis factor-α
  • vascular endothelial cells

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