Mechanical loading and injury induce human myotubes to release neutrophil chemoattractants Article (Faculty180)

cited authors

  • Tsivitse, Susan K; Mylona, Eleni; Peterson, Jennifer M; Gunning, William T; Pizza, Francis X

description

  • The purpose of this study was to 1) test the hypothesis that skeletal muscle cells (myotubes) after mechanical loading and/or injury are a source of soluble factors that promote neutrophil chemotaxis and superoxide anion (O(2)(-).) production and 2) determine whether mechanical loading and/or injury causes myotubes to release cytokines that are known to influence neutrophil responses [tumor necrosis factor-alpha (TNF-alpha), IL-8, and transforming growth factor-beta1 (TGF-beta1)]. Human myotubes were grown in culture and exposed to either a cyclic strain (0, 5, 10, 20, or 30% strain) or a scrape injury protocol. Protocols of 5, 10, and 20% strain did not cause injury, whereas 30% strain and scrape injury caused a modest and a high degree of injury, respectively. Conditioned media from strained myotubes promoted chemotaxis of human blood neutrophils and primed them for O(2)(-). production in a manner that was dependent on a threshold of strain and independent from injury. Neutrophil chemotaxis, but not priming, progressively increased with higher magnitudes of strain. Conditioned media only from scrape-injured myotubes increased O(2)(-). production from neutrophils. Concentrations of IL-8 and total TGF-beta1 in conditioned media were reduced by mechanical loading, whereas TNF-alpha and active TGF-beta1 concentrations were unaffected. In conclusion, skeletal muscle cells after mechanical loading and injury are an important source of soluble factors that differentially influence neutrophil chemotaxis and the stages of neutrophil-derived reactive oxygen species production. Neutrophil responses elicited by mechanical loading, however, did not parallel changes in the release of IL-8, TGF-beta1, or TNF-alpha from skeletal muscle cells.

authors

publication date

  • 2005

published in

start page

  • C721

end page

  • 9

volume

  • 288