| Autor: |
Docagne, Fabian, Campbell, Sandra J., Bristow, Adrian F., Poole, Stephen, Vigues, Stephan, Guaza, Carmen, Perry, V. Hugh, Anthony, Daniel C. |
| Předmět: |
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| Zdroj: |
European Journal of Neuroscience; Mar2005, Vol. 21 Issue 5, p1205-1214, 10p |
| Abstrakt: |
Most pathologies of the brain have an inflammatory component, associated with the release of cytokines such as interleukin-1β (IL-1β) from resident and infiltrating cells. The IL-1 type I receptor (IL-1RI) initiates a signalling cascade but the type II receptor (IL-1RII) acts as a decoy receptor. Here we have investigated the expression of IL-1β, IL-1RI and IL-1RII in distinct inflammatory lesions in the rat brain. IL-1β was injected into the brain to generate an inflammatory lesion in the absence of neuronal cell death whereas neuronal death was specifically induced by the microinjection ofN-methyl-d-aspartate (NMDA). Using TaqMan RT-PCR and ELISA, we observed elevatedde novoIL-1β synthesis 2 h after the intracerebral microinjection of IL-1β; thisde novoIL-1β remained elevated 24 h later. There was a concomitant increase in IL-1RI mRNA but a much greater increase in IL-1RII mRNA. Immunostaining revealed that IL-1RII was expressed on brain endothelial cells and on infiltrating neutrophils. In contrast, although IL-1β and IL-1RI were elevated to similar levels in response to NMDA challenge, the response was delayed and IL-1RII mRNA expression was unchanged. The lesion-specific expression of IL-1 receptors suggests that the receptors are differentially regulated in a manner not directly related to the endogenous level of IL-1 in the CNS. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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