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Most pathologies of the brain have an inflammatory component, associated with the release of cytokines such as interleukin-1beta (IL-1beta) 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-1beta, IL-1RI and IL-1RII in distinct inflammatory lesions in the rat brain. IL-1beta 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 of N-methyl-D-aspartate (NMDA). Using TaqMan RT-PCR and ELISA, we observed elevated de novo IL-1beta synthesis 2 h after the intracerebral microinjection of IL-1beta; this de novo IL-1beta 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-1beta 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.

Original publication




Journal article


Eur J Neurosci

Publication Date





1205 - 1214


Animals, Blotting, Western, Chemokines, CXC, Encephalitis, Enzyme-Linked Immunosorbent Assay, Gene Expression Regulation, Immunohistochemistry, Immunoprecipitation, Intercellular Signaling Peptides and Proteins, Interleukin-1, Male, N-Methylaspartate, RNA, Messenger, Rats, Rats, Wistar, Receptors, Interleukin-1, Receptors, Interleukin-1 Type I, Receptors, Interleukin-1 Type II, Reverse Transcriptase Polymerase Chain Reaction, Statistics, Nonparametric, Time Factors