• Shinichirou Yoshida, Yoshihiro Hagiwara, Masahiro Tsuchiya, Masamichi Shinoda, Masashi Koide, Hiroyasu Hatakeyama, Chayanit Chaweewannakorn, Toshihisa Yano, Yasuhito Sogi, Nobuyuki Itaya, Takuya Sekiguchi, Yutaka Yabe, Keiichi Sasaki, Makoto Kanzaki, and Eiji Itoi.
• 1 Department of Orthopaedic Surgery, Tohoku University Graduate School of Medicine, Sendai, Japan.
• Mol Pain. 2018 Jan 1; 14: 1744806918757286.

AbstractMuscle pain is a common condition that relates to various pathologies. Muscle overuse induces muscle pain, and neutrophils are key players in pain production. Neutrophils also play a central role in chronic pain by secreting interleukin (IL)-18. The aim of this study was to investigate the involvement of neutrophils and IL-18 in a mouse model of muscle pain. The right hind leg muscles of BALB/c mice were stimulated electrically to induce excessive muscle contraction. The left hind leg muscles were not stimulated. The pressure pain threshold, number of neutrophils, and IL-18 levels were investigated. Furthermore, the effects of the IL-18-binding protein and Brilliant Blue G on pain were investigated. In stimulated muscles, pressure pain thresholds decreased, and neutrophil and IL-18 levels increased compared with that in non-stimulated muscles. The administration of IL-18-binding protein and Brilliant Blue G attenuated hyperalgesia caused by excessive muscle contraction. These results suggest that increased IL-18 secretion from larger numbers of neutrophils elicits mechanical hyperalgesia.

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