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      Exercise and IL-6 infusion inhibit endotoxin-induced TNF-alpha production in humans.

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          Abstract

          During "nondamaging" exercise, skeletal muscle markedly releases interleukin (IL)-6, and it has been suggested that one biological role of this phenomenon is to inhibit the production of tumor necrosis factor (TNF)- alpha, which is known to cause pathogenesis such as insulin resistance and atherosclerosis. To test this hypothesis, we performed three experiments in which eight healthy males either rested (CON), rode a bicycle for 3 h (EX), or were infused with recombinant human IL-6 (rhIL-6) for 3 h while they rested. After 2.5 h, the volunteers received a bolus of Escherichia coli lipopolysaccharide endotoxin (0.06 ng/kg) i.v. to induce low-grade inflammation. In CON, plasma TNF-alpha increased significantly in response to endotoxin. In contrast, during EX, which resulted in elevated IL-6, and rhIL-6, the endotoxin-induced increase in TNF-alpha was totally attenuated. In conclusion, physical exercise and rhIL-6 infusion at physiological concentrations inhibit endotoxin-induced TNF-alpha production in humans. Hence, these data provide the first experimental evidence that physical activity mediates antiinflammatory activity and suggest that the mechanism include IL-6, which is produced by and released from exercising muscles.

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          Author and article information

          Journal
          FASEB J
          FASEB journal : official publication of the Federation of American Societies for Experimental Biology
          Wiley
          1530-6860
          0892-6638
          May 2003
          : 17
          : 8
          Affiliations
          [1 ] Department of Infectious Diseases, Rigshospitalet, University of Copenhagen, Denmark.
          Article
          02-0670fje
          10.1096/fj.02-0670fje
          12626436
          6717cc09-e75a-4fd6-a299-3b6145dd92af

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