| First Author | Wheeler RD | Year | 2003 |
| Journal | J Neurochem | Volume | 85 |
| Issue | 6 | Pages | 1412-20 |
| PubMed ID | 12787061 | Mgi Jnum | J:126730 |
| Mgi Id | MGI:3761919 | Doi | 10.1046/j.1471-4159.2003.01787.x |
| Citation | Wheeler RD, et al. (2003) Interleukin-18 induces expression and release of cytokines from murine glial cells: interactions with interleukin-1 beta. J Neurochem 85(6):1412-20 |
| abstractText | 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-1 alpha and proIL-1 beta, and release of IL-6 from mixed glia. Treatment of lipopolysaccharide-primed microglia with adenosine triphosphate (ATP), an endogenous secondary stimulus, induced IL-1 beta and IL-18 release. Although deletion of the IL-18 gene did not affect IL-1 beta expression or release in this experimental paradigm, IL-1 beta knockout microglia released significantly less IL-18 compared to wild-type microglia. In addition, ATP induced release of mature IL-1 beta 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-1 beta differ in their regulation and actions. |
