The effects of exercise on macrophage function

DOI Web Site 被引用文献2件 参考文献132件
  • Kizaki Takako
    Department of Molecular Predictive Medicine and Sport Science, Kyorin University, School of Medicine
  • Sato Shogo
    Department of Molecular Predictive Medicine and Sport Science, Kyorin University, School of Medicine
  • Sakurai Takuya
    Department of Molecular Predictive Medicine and Sport Science, Kyorin University, School of Medicine
  • Ogasawara Junetsu
    Department of Molecular Predictive Medicine and Sport Science, Kyorin University, School of Medicine
  • Imaizumi Kazuhiko
    Laboratory of Physiological Sciences, Faculty of Human Sciences, Waseda University
  • Izawa Tetsuya
    Faculty of Health and Sport Science, Doshisha University
  • Nagasawa Junichi
    Department of Applied Physics and Chemistry, The University of Electro-Communications
  • Saitoh Daizo
    Division of Traumatology, National Defense Medical College Research Institute
  • Haga Shukoh
    Graduate School of Comprehensive Human Sciences, University of Tsukuba
  • Ohno Hideki
    Department of Molecular Predictive Medicine and Sport Science, Kyorin University, School of Medicine

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Innate immunity is our first line of defense against infectious pathogens. One of the major constituents of the innate immune system is macrophages that perform important phagocytic, regulatory and antigen presentation functions. Physically active individuals are reportedly less susceptible than sedentary individuals to viral and bacterial infections, suggesting that exercise improves immune function. Exercise increases the release of catecholamines, glucocorticoids and other factors that have immunomodulatory effects. For example, proinflammatory cytokine production from macrophages was inhibited by β2-adrenergic receptor (β2AR) agonist catecholamines, but exercise training down-regulated the expression of β2AR in macrophages, improving innate immune functions. In addition, the generation of suppressor macrophages by glucocorticoids that are normally induced during acute cold stress was inhibited in swimming-trained mice. Also, an inactive lifestyle leads to the accumulation of visceral fat, which is accompanied by adipose tissue infiltration by pro-inflammatory immune cells, mainly macrophages, and the development of a low-grade systemic inflammatory state. Exercise decreases chronic low-grade systemic inflammation and improves insulin sensitivity in obese individuals. Although the mechanisms behind these favorable effects of exercise are not fully understood, recent studies have shown that exercise training prevents adipose tissue infiltration by pro-inflammatory macrophages and that ghrelin expressed in macrophages functions as a mediator of the anti-inflammatory effects of exercise training. In this Review, the authors focus on the known mechanisms by which exercise exerts its effects on macrophages, and discuss the implications of these effects for the prevention and treatment of disease.

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