IL-17, neutrophil activation and muscle damage following endurance exercise

Kaoru Sugama, Katsuhiko Suzuki*, Kayo Yoshitani, Koso Shiraishi, Takashi Kometani

*この研究の対応する著者

研究成果: Article査読

43 被引用数 (Scopus)

抄録

The T-cell subset Th17 is induced partly by interleukin (IL)-6 and activated by IL- 23, and produces a proinflammatory cytokine IL-17. Since IL-6 increases dramatically following long-lasting endurance exercise, this response may also stimulate the induction of IL-17 and IL-23 after exercise. The aim of this study was to clarify the dynamics of IL-17 in association with endurance exercise-induced muscle damage and inflammatory responses. Fourteen male triathletes participated in a duathlon race consisting of 5 km of running, 40 km of cycling and 5 km of running. Venous blood and urine samples were collected before, immediately after, 1.5 h and 3 h after the race. Plasma and urine were analyzed using enzyme-linked immunosorbent assays (ELISA). Haematological and biochemical variables such as neutrophil activation marker (myeloperoxidase: MPO), muscle damage marker (myoglobin: Mb) and soluble receptor activator of nuclear factor (NF)-κB ligand (sRANKL) were also determined to estimate the biological and pathological significance. Plasma concentrations of IL-6 (+26.0×), MPO (+3.2×) and Mb (+4.9×) increased significantly immediately after the race and IL-17 and IL-23 tended to increase. Furthermore, plasma concentrations of IL-12p40 and sRANKL increased significantly after the race. The measured parameters related to Th17 cytokines in the urinary output were closely correlated with each other and muscle damage marker. These findings suggest that IL-17 induced by IL-6 and activated by IL-23 or other IL-17 producing-cells and IL-23 might promote neutrophil activation and muscle damage following prolonged endurance exercise.

本文言語English
ページ(範囲)115-126
ページ数12
ジャーナルExercise immunology review
18
出版ステータスPublished - 2012

ASJC Scopus subject areas

  • 免疫学

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