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- W1996363544 abstract "Tumor necrosis factor-α (TNF-α), a mononuclear phagocyte-derived peptide is known to participate in the pathogenesis of fever. To determine whether a feedback mechanism exists by which elevated temperatures influence TNF-α generation, we have examined the effects of heat shock on the in vitro synthesis of TNF-α by rat glomeruli, inflammatory peritoneal macrophages and blood monocytes. Preexposure of peritoneal macrophages to elevated temperatures for 20 min decreased the subsequent lipopolysaccharide-induced release of TNF-α bioactivity. The mean reductions were 11.9 ± 86.3 ± 12.0, and 95.2 ± 3.5% after pretreatment at 39, 41 and 43°C, respectively. Reductions, that were transient, were maximum when lipopolysaccharide was added 0–2 h after heat shock. They correlated with the decreased release of immunoreactive TNF-α and the decreased expression of both cell-associated TNF-α molecule and TNF-α mRNA. Heat shock-induced inhibition of TNF-α release was independent of variations of prostaglandin synthesis, but was possibly related to the induction of heat-shock proteins since (a) macrophages exposed to heat shock synthesized the major 70- and 90-kDa heat-shock proteins, and (b) chemical inducers of the heat-shock response were also effective inhibitors of TNF-α release. The mean reduction of TNF-α release after pretreatment at 41°C was found to be identical in glomerular tissue (82.0 ± 7.5%), but significantly less in blood monocytes (43.9 ± 10.9%). This supports the hypothesis that a negative-feedback mechanism exists between elevated temperature and lipopolysaccharide-induced TNF-α synthesis, and suggests that this regulation is less active in blood monocytes than in tissue macrophages." @default.
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- W1996363544 date "1992-11-01" @default.
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- W1996363544 title "Heat shock prevents lipopolysaccharide-induced tumor necrosis factor-α synthesis by rat mononuclear phagocytes" @default.
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- W1996363544 doi "https://doi.org/10.1002/eji.1830221133" @default.
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