TY - JOUR
T1 - Involvement of neutrophils and interleukin-18 in nociception in a mouse model of muscle pain
AU - Yoshida, Shinichirou
AU - Hagiwara, Yoshihiro
AU - Tsuchiya, Masahiro
AU - Shinoda, Masamichi
AU - Koide, Masashi
AU - Hatakeyama, Hiroyasu
AU - Chaweewannakorn, Chayanit
AU - Yano, Toshihisa
AU - Sogi, Yasuhito
AU - Itaya, Nobuyuki
AU - Sekiguchi, Takuya
AU - Yabe, Yutaka
AU - Sasaki, Keiichi
AU - Kanzaki, Makoto
AU - Itoi, Eiji
N1 - Publisher Copyright:
© The Author(s) 2018.
PY - 2018/1/1
Y1 - 2018/1/1
N2 - Muscle 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.
AB - Muscle 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.
KW - Electrical stimulation
KW - Interleukin-18
KW - Mechanical hyperalgesia
KW - Muscle pain
KW - Neutrophil
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U2 - 10.1177/1744806918757286
DO - 10.1177/1744806918757286
M3 - Article
C2 - 29353540
AN - SCOPUS:85041385157
SN - 1744-8069
VL - 14
JO - Molecular Pain
JF - Molecular Pain
ER -