title: Exhaustive exercise reduces tumor necrosis factor-alpha production in response to lipopolysaccharide in mice.
abstract: OBJECTIVE
  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)-alpha concentration in response to LPS.
  
  
  METHODS
  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-alpha mRNA expression. Blood and tissue samples were collected for determination of TNF-alpha and TNF receptors (TNFR) 1 h after the LPS injection.
  
  
  RESULTS
  Although there was a significant suppression in LPS-induced plasma TNF-alpha 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-alpha mRNA expression and TNFR content in tissues between the Ex and Non-Ex groups. Interestingly, TNF-alpha 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).
  
  
  CONCLUSIONS
  These data suggest that exhaustive exercise-induced suppression of the plasma TNF-alpha concentration despite LPS stimulation might depend on translation of TNF-alpha in tissues.
authors.affiliation: Department of Health and Sports Science, Kawasaki University of Medical Welfare, Kurashiki, Japan.
authors.forename: Yohei
authors.initials: Y
authors.lastname: Tanaka
authors.forename: Noriaki
authors.initials: N
authors.lastname: Kawanishi
authors.forename: Daisuke
authors.initials: D
authors.lastname: Shiva
authors.forename: Noritsugu
authors.initials: N
authors.lastname: Tsutsumi
authors.forename: Masataka
authors.initials: M
authors.lastname: Uchida
authors.forename: Hiromi
authors.initials: H
authors.lastname: Kitamura
authors.forename: Yasuko
authors.initials: Y
authors.lastname: Kato
authors.forename: Hiromi
authors.initials: H
authors.lastname: Yano
mesh_terms: D000818:Animals; D001424:Bacterial Infections / Q000276:immunology* / Q000503:physiopathology; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000276:immunology; D005080:Exercise Test; D005786:Gene Expression Regulation / Q000276:immunology; D007108:Immune Tolerance / Q000502:physiology*; D007109:Immunity / Q000502:physiology*; D008070:Lipopolysaccharides / Q000633:toxicity; D008264:Macrophages / Q000276:immunology; D008297:Male; D051379:Mice; D008809:Mice, Inbred C3H; D009000:Monocytes / Q000276:immunology; D010805:Physical Conditioning, Animal / Q000009:adverse effects*; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000235:genetics / Q000378:metabolism; D013312:Stress, Physiological / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis / Q000097:blood* / Q000235:genetics
chemical_list: D008070:Lipopolysaccharides; D047888:Receptors, Tumor Necrosis Factor, Type I; C506236:Tnfrsf1a protein, mouse; D014409:Tumor Necrosis Factor-alpha