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. 2020;39(2):39-52.
doi: 10.1080/08830185.2019.1682569. Epub 2019 Nov 4.

Anti-Inflammatory Effect of Exercise Mediated by Toll-Like Receptor Regulation in Innate Immune Cells - A Review

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Anti-Inflammatory Effect of Exercise Mediated by Toll-Like Receptor Regulation in Innate Immune Cells - A Review

Nicolas Collao et al. Int Rev Immunol. 2020.

Abstract

Over the last three decades, the combination of a sedentary lifestyle and excessive food intake has led to a significant increase in the prevalence of obesity. The latter favors a chronic low-grade inflammatory state and an over-activation of the innate immune system, which contribute to insulin resistance and type 2 diabetes. Physical exercise is a powerful preventive tool and treatment for several diseases as it induces metabolic and immune effects that provide health benefits. Exercise is known to reduce inflammation; however, the underlying mechanisms responsible are not fully elucidated. One proposed mechanism is a reduced expression and/or activation of pro-inflammatory toll-like receptors (TLRs) on innate immune cells after exercise, which could contribute to the protective effect of exercise against insulin resistance and the prevention of the development of metabolic diseases. The aim of the present study is therefore to review the current evidence about the anti-inflammatory effects of exercise and toll-like receptors regulation on immune cells in humans.Key PointsObesity leads to a low-grade chronic inflammatory state and an over-activation of the innate immune system that is directly involved in the develop metabolic syndrome.The anti-inflammatory effect of exercise has been previously suggested through the reduction of the expression and/or activation of pro-inflammatory toll-like receptors (TLRs) in innate immune cells, which represent one of the main inflammatory responses triggered by obesityThe underlying mechanisms in which toll-like receptors expression modulate the reduction of chronic inflammation are not fully elucidated.

Keywords: Physical activity; cytokines; diabetes; inflammation; metabolic syndrome; obesity.

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