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  • Title: Response of interleukin-6-deficient mice to tumor necrosis factor-induced metabolic changes and lethality.
    Author: Libert C, Takahashi N, Cauwels A, Brouckaert P, Bluethmann H, Fiers W.
    Journal: Eur J Immunol; 1994 Sep; 24(9):2237-42. PubMed ID: 7522168.
    Abstract:
    Whether interleukin (IL)-6 contributes to tumor necrosis factor (TNF)-induced lethal shock or whether, on the contrary, it is part of a protective feedback system, remains unresolved. Here, we report experiments with IL-6 gene-disrupted mice (IL-6(0/0)). We have tested the susceptibility of these to TNF-induced metabolic changes and lethality in different models, and compared the results with those obtained with IL-6+/+ wild-type mice. We studied the response to TNF in three different models: (i) murine TNF administration; (ii) TNF in galactosamine (GalN)-sensitized mice; (iii) TNF in Bacillus Calmette-Guérin-sensitized mice. We observed no significant difference between the two types of mice in any of the three models. Furthermore, IL-6(0/0) mice could be equally well desensitized (by IL-1) to TNF/GalN-induced lethality and tolerized to TNF-induced shock as IL-6+/+ mice. We also observed that, in response to turpentine, TNF or IL-1, IL-6(0/0) mice produced significantly less acute phase proteins (APP) than IL-6+/+ mice. In IL-6(0/0) mice, less corticosterone was induced by TNF than in the control mice, while the response to adrenocorticotropic hormone was the same. The results indicate that IL-6 is not contributing in a major way to the pathogenesis leading to TNF-induced shock, and that neither IL-6 nor the APP studied are essential for a protective feedback system.
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