Differential regulation of type I and type II interleukin-1 receptors in focal brain inflammation.
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 recept...
| Asıl Yazarlar: | , , , , , , , |
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| Materyal Türü: | Journal article |
| Dil: | English |
| Baskı/Yayın Bilgisi: |
2005
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| _version_ | 1826266453687402496 |
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| author | Docagne, F Campbell, S Bristow, A Poole, S Vigues, S Guaza, C Perry, V Anthony, D |
| author_facet | Docagne, F Campbell, S Bristow, A Poole, S Vigues, S Guaza, C Perry, V Anthony, D |
| author_sort | Docagne, F |
| collection | OXFORD |
| description | 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. |
| first_indexed | 2024-03-06T20:39:11Z |
| format | Journal article |
| id | oxford-uuid:33b0e711-26d1-4ef8-be8e-b28e0a14c596 |
| institution | University of Oxford |
| language | English |
| last_indexed | 2024-03-06T20:39:11Z |
| publishDate | 2005 |
| record_format | dspace |
| spelling | oxford-uuid:33b0e711-26d1-4ef8-be8e-b28e0a14c5962022-03-26T13:21:36ZDifferential regulation of type I and type II interleukin-1 receptors in focal brain inflammation.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:33b0e711-26d1-4ef8-be8e-b28e0a14c596EnglishSymplectic Elements at Oxford2005Docagne, FCampbell, SBristow, APoole, SVigues, SGuaza, CPerry, VAnthony, DMost 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. |
| spellingShingle | Docagne, F Campbell, S Bristow, A Poole, S Vigues, S Guaza, C Perry, V Anthony, D Differential regulation of type I and type II interleukin-1 receptors in focal brain inflammation. |
| title | Differential regulation of type I and type II interleukin-1 receptors in focal brain inflammation. |
| title_full | Differential regulation of type I and type II interleukin-1 receptors in focal brain inflammation. |
| title_fullStr | Differential regulation of type I and type II interleukin-1 receptors in focal brain inflammation. |
| title_full_unstemmed | Differential regulation of type I and type II interleukin-1 receptors in focal brain inflammation. |
| title_short | Differential regulation of type I and type II interleukin-1 receptors in focal brain inflammation. |
| title_sort | differential regulation of type i and type ii interleukin 1 receptors in focal brain inflammation |
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