Muscle pain is a very 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-18. The aim of this study was to investigate the involvement of neutrophils and interleukin-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 interleukin-18 levels were investigated. Furthermore, the effects of the interleukin-18-binding protein and Brilliant Blue G on pain were investigated. In stimulated muscles, pressure pain thresholds decreased and neutrophil and interleukin-18 levels increased compared with non-stimulated muscles. Interleukin-18-binding protein and Brilliant Blue G administration attenuated hyperalgesia caused by excessive muscle contraction. These results suggest that increased interleukin-18 secreted from increased numbers of neutrophils produce mechanical hyperalgesia.
doi: 10.1177/1744806918757286.
PMID: 29353540
Yoshida S, Hagiwara Y, Tsuchiya M, Shinoda M, Koide M, Hatakeyama H, Chaweewannakorn C, Yano T, Sogi Y, Itaya N, Sekiguchi T, Yabe Y, Sasaki K, Kanzaki M, Itoi E.
