Intercellular adhesion molecule-1 expression induced by interleukin (IL)-1β or an IL-1β fragment is blocked by an IL-1 receptor antagonist and a soluble IL-1 receptor

Lielie Hong, Luca Imeri, Mark R. Opp, Arnold Postlethwaite, Jerome M. Seyer, James M. Krueger

Research output: Contribution to journalArticle

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Abstract

The effects of a recombinant human interleukin-1 (IL-1) receptor antagonist (IL-1ra) and a recombinant human soluble IL-1 receptor (sIL-1R) on cytokine-induced intercellular adhesion molecule-1 (ICAM-1) expression in a human glioblastoma cell line and a neuroblastoma cell line were determined. Cells were incubated with IL-1β, tumor necrosis factor (TNF)α and interferon (IFN)γ. Cells were also tested under identical conditions with an IL-1β synthetic peptide fragment (IL-1β208-240) previously shown to possess biological activity. IL-1β, TNFα and IFNγ potentiated ICAM-1 expression in both cell lines in a dose-related manner. The IL-1β208-240 fragments, corresponding to the rabbit, rat and human sequences, enhanced ICAM-1 expression in glioblastoma cells at high doses. ICAM-1 expression induced by IL-1β, rabbit IL-1β208-240 and human IL-1β208-240 was blocked by the IL-1ra, while TNFα- and IFNγ-induced ICAM-1 expression were not. ICAM-1 expression induced by IL-1β and human IL-1β208-240 was also blocked by the sIL-1R. Our findings suggest that IL1β208-240 acts as an IL-1β agonist in enhancing ICAM-1 expression in vitro and that this effect is receptor-mediated.

Original languageEnglish (US)
Pages (from-to)163-170
Number of pages8
JournalJournal of Neuroimmunology
Volume44
Issue number2
DOIs
StatePublished - Jan 1 1993

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Interleukin-1 Receptors
Intercellular Adhesion Molecule-1
Interleukin-1
Interleukins
Interferons
Tumor Necrosis Factor-alpha
Glioblastoma
Cell Line
Rabbits
Peptide Fragments
Neuroblastoma
Cytokines

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

Cite this

Intercellular adhesion molecule-1 expression induced by interleukin (IL)-1β or an IL-1β fragment is blocked by an IL-1 receptor antagonist and a soluble IL-1 receptor. / Hong, Lielie; Imeri, Luca; Opp, Mark R.; Postlethwaite, Arnold; Seyer, Jerome M.; Krueger, James M.

In: Journal of Neuroimmunology, Vol. 44, No. 2, 01.01.1993, p. 163-170.

Research output: Contribution to journalArticle

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