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Interleukin‐18 induces expression and release of cytokines from murine glial cells: interactions with interleukin‐1β
Author(s) -
Wheeler Rachel D.,
Brough David,
Le Feuvre Rosalind A.,
Takeda Kiyoshi,
Iwakura Yoichiro,
Luheshi Giamal N.,
Rothwell Nancy J.
Publication year - 2003
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2003.01787.x
Subject(s) - microglia , proinflammatory cytokine , cytokine , biology , interleukin , microbiology and biotechnology , inflammation , mediator , lipopolysaccharide , interleukin 4 , immunology
Interleukin (IL)‐18, a member of the IL‐1 cytokine family, is an important mediator of peripheral inflammation and host defence responses. IL‐1 is a key proinflammatory cytokine in the brain, but the role of IL‐18 in the CNS is not yet clear. The objective of this study was to investigate the actions of IL‐18 on mouse glial cells. IL‐18 induced intracellular expression of IL‐1α and proIL‐1β, and release of IL‐6 from mixed glia. Treatment of lipopolysaccharide‐primed microglia with adenosine triphosphate (ATP), an endogenous secondary stimulus, induced IL‐1β and IL‐18 release. Although deletion of the IL‐18 gene did not affect IL‐1β expression or release in this experimental paradigm, IL‐1β knockout microglia released significantly less IL‐18 compared to wild‐type microglia. In addition, ATP induced release of mature IL‐1β from IL‐18‐primed microglia. These data suggest that IL‐18 may contribute to inflammatory responses in the brain, and demonstrate that, in spite of several common features, IL‐18 and IL‐1β differ in their regulation and actions.