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Título: | Differential regulation of type I and type II interleukin-1 receptors in focal brain inflammation |
Autor: | Docagne, Fabian CSIC ORCID; Campbell, S. J.; Bristow, A. F.; Poole, S.; Vigues, Stephan; Guaza, Carmen CSIC ORCID ; Perry, V. H.; Anthony, D. C. | Fecha de publicación: | 2005 | Editor: | Blackwell Publishing | Citación: | European Journal of Neuroscience 21: 1205-1214 (2005) | Resumen: | 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 of N-methyl-D-aspartate (NMDA). Using TaqMan RT-PCR and ELISA, we observed elevated de novo IL-1β synthesis 2 h after the intracerebral microinjection of IL-1β; this de novo IL-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. | URI: | http://hdl.handle.net/10261/73256 | DOI: | 10.1111/j.1460-9568.2005.03965.x | Identificadores: | doi: 10.1111/j.1460-9568.2005.03965.x issn: 0953-816X |
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