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• W2010497366 abstract "<i>Objective:</i> Stressful exercise reduces the plasma pro-inflammatory cytokine concentration in response to lipopolysaccharide (LPS). The aim of this study was to clarify the mechanism of exhaustive exercise-induced suppression of the plasma tumor necrosis factor (TNF)-α concentration in response to LPS. <i>Methods:</i> Male C3H/HeN mice (n = 66) were randomized to treadmill running to exhaustion (Ex) or a sedentary (Non-Ex) condition. Monocytes and splenic macrophages were collected from some animals, and other animals were injected with LPS (1 mg/kg) immediately after the exercise. The liver, lung and spleen tissues in the mice were removed 30 min after the LPS injection for determination of TNF-α mRNA expression. Blood and tissue samples were collected for determination of TNF-α and TNF receptors (TNFR) 1 h after the LPS injection. <i>Results:</i> Although there was a significant suppression in LPS-induced plasma TNF-α in the Ex mice when compared to the Non-Ex mice (p < 0.01), soluble TNFR in plasma was not affected by the exercise. There was no change in cell-surface expression of Toll-like receptor 4 (TLR4) and in LPS-induced TNF-α mRNA expression and TNFR content in tissues between the Ex and Non-Ex groups. Interestingly, TNF-α contents in the liver, lung and spleen of the Ex mice were significantly lower than those of the Non-Ex group (p < 0.01, p < 0.01 and p < 0.05, respectively). <i>Conclusion:</i> These data suggest that exhaustive exercise-induced suppression of the plasma TNF-α concentration despite LPS stimulation might depend on translation of TNF-α in tissues." @default.
• W2010497366 created "2016-06-24" @default.
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• W2010497366 date "2010-01-01" @default.
• W2010497366 modified "2023-10-17" @default.
• W2010497366 title "Exhaustive Exercise Reduces Tumor Necrosis Factor-α Production in Response to Lipopolysaccharide in Mice" @default.
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• W2010497366 doi "https://doi.org/10.1159/000290044" @default.
• W2010497366 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/20203534" @default.
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