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Interleukin-1-mediated febrile responses in mice and inter-leukin-1 beta activation of NFB in mouse primary astrocytes, involves the interleukin-1 receptor accessory protein |
European Cytokine Network. Volume 9, Number 2, 131-8, June 1998, Articles originaux
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 Free Article
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Author(s) : M. Zetterström, J. Lundkvist, D. Malinowski, G. Eriksson, T. Bartfai |
Summary : The endogenous pyrogen interleukin-1 (IL-1) is considered as one of the key molecules in orchestrating the host response of injury and inflammation. IL-1 exerts its effects upon binding to the type I IL-1 receptor (IL-1RI). The IL-1-IL-1RI complex is further thought to associate with the IL-1 receptor accessory protein (IL-1RAcP), which is suggested to be important for most IL-1 signal transduction pathways. With the aim of investigating the importance of the IL-1RAcP in IL-1 signalling, IL-1 and IL-1 induced febrile responses and IL-1-mediated activation of NFB in primary astrocyte cultures were examined using IL-1RAcP-deficient (IL-1RAcP KO) and wild type mice, respectively. It was shown that neither recombinant rat IL-1 (rrIL-1, 25 g/kg), recombinant rat IL-1 (rrIL-1, 40 g/kg) nor recombinant human IL-1 (rhIL-1, 50 g/kg) injected i.p. could elicit febrile responses in the IL-1RAcP-deficient mice, while the same doses of rrIL-1/or rhIL-1 injected into wild type mice caused normal fever responses. A febrile response could be induced in the IL-1RAcP-deficient mice by i.p. administration of E. coli lipopolysaccharide (LPS, 50 g/kg) and this response was similar to that obtained in wild type mice. Furthermore, it was shown that rhIL-1 activated, in a concentration-dependent manner, nuclear translocation of the transcriptional nuclear factor kappa B (NFB) in primary astrocyte cultures prepared from wild type mice, whereas no IL-1-induced translocation of NFB could be detected in cultures prepared from IL-1RAcP-deficient mice, as revealed by electrophoretic mobility shift assay (EMSA). The rhIL-1-induced NFB complexes were shown to contain p50 but no, or very little, p65 and cRel immunoreactive proteins. |
Keywords : interleukin-1, IL-1 receptor accessory protein, fever, NFB, CNS. |
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