Inteferon-γ potentiates interleukin (IL)-6 and tumor necrosis factor- α but not IL-1β induced by endotoxin in the brain

M. G. De Simoni, L. Terreni, R. Chiesa, F. Mangiarotti, G. L. Forloni

Research output: Contribution to journalArticlepeer-review

Abstract

Because interferon-γ (IFNγ) is present in the central nervous system during neurologic diseases associated with inflammation, its effect on endotoxin-induced cytokines was studied. Cerebrospinal fluid (CSF) and serum levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNFα), their messenger RNA expression in brain areas (hypothalamus, hyppocampus, and striatum) and in spleen were evaluated 2 and 8 h after endotoxin [lipopolysaccharide (LPS), 25 μg/rat icv], IFNγ (2.5 μg/rat icv) or after their coadministration in rats. CSF and serum IL-1β levels were increased by LPS alone and IFNγ co-administration did not furtherly increase them. IFNγ potentiated LPS effect on IL-6 and TNFα levels in both CSF and serum. LPS and IFN-γ coadministration did not alter IL-1β messenger RNA expression induced by LPS in brain areas and in spleen, but it potentiated that of IL-6 and TNFα. The present in vive data show that icv coadministration of LPS and IFNγ results in a potentiation of cytokine production (IL-6 and TNFα) which may trigger a cascade of events relevant to neurodegenerative processes. This action is independent of IL-1β because the production of this cytokine is not altered by IFNγ treatment.

Original languageEnglish
Pages (from-to)5220-5226
Number of pages7
JournalEndocrinology
Volume138
Issue number12
Publication statusPublished - 1997

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

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