Delineation of the Proinflammatory Cytokine Cascade in Fever Inductiona
| Autor: | M Zetterström, Tamas Bartfai, Pernilla Östlund, Anna K. Sundgren-Andersson |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
Lipopolysaccharides
Fever Sialoglycoproteins Inflammation General Biochemistry Genetics and Molecular Biology Proinflammatory cytokine Mice History and Philosophy of Science medicine Animals Beta (finance) Interleukin 6 Receptor Mice Knockout biology Interleukin-6 Chemistry General Neuroscience Receptors Interleukin-1 Interleukin Interleukin 1 Receptor Antagonist Protein Immunology biology.protein Cytokines Interleukin 18 Tumor necrosis factor alpha medicine.symptom Interleukin-1 |
| Zdroj: | Annals of the New York Academy of Sciences. 856:48-52 |
| ISSN: | 1749-6632 0077-8923 |
| Popis: | Bacterial lipopolypolysaccharide (LPS)-induced fever involves induction of the proinflammatory cytokines interleukin (IL)-1 alpha, IL-1 beta, tumor necrosis factor-alpha (TNF-alpha), and IL-6, both in the periphery and in the brain. These molecules can induce expression of each other and also regulate expression of their own receptors in a complex manner. The functional hierarchy of these highly inducible proteins is therefore difficult to determine. Using mice strains carrying the null mutations of IL-1 beta, IL-1RI, IL-1RAcP, or IL-6, respectively, we show that LPS-induced fever involves IL-1 beta, which acts at a complex consisting of the type I IL-1 receptor and the IL-1RAcP. This action occurs prior to central IL-6 release, which has been shown to be a necessary component of fever responses induced by LPS, IL-1 beta, and also TNF-alpha. In the absence of IL-1 beta, as in IL-1 beta-deficient mice, LPS, IL-1 alpha, and IL-1 beta cause hyperresponsive fevers when exogenously applied. Murine TNF-alpha is a poor pyrogen in mice even when mice are kept at thermoneutral temperature (30 degrees C). TNF-alpha-mediated fever depends on central IL-6 expression. |
| Databáze: | OpenAIRE |
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