ヤマウチ　カヅヨ   YAMAUCHI Kadzuyo   山内　かづ代    所属   医学部 医学科    職種   評議員
論文種別	原著
言語種別	英語
査読の有無	査読あり
表題	Interleukin-6 and interleukin-6 receptor expression, localization, and involvement in pain-sensing neuron activation in a mouse intervertebral disc injury model.
掲載誌名	正式名：Journal of orthopaedic research : official publication of the Orthopaedic Research Society 略　 称：J Orthop Res ISSNコード：(1554-527X)0736-0266(Linking)
掲載区分	国外
巻・号・頁	33(10),pp.1508-14
著者・共著者	Sainoh Takeshi, Orita Sumihisa, Miyagi Masayuki, Sakuma Yoshihiro, Yamauchi Kazuyo, Suzuki Miyako, Kubota Go, Oikawa Yasuhiro, Inage Kazuhide, Sato Jun, Fujimoto Kazuki, Shiga Yasuhiro, Inoue Gen, Aoki Yasuchika, Takahashi Kazuhisa, Ohtori Seiji
発行年月	2015/10
概要	The pathological mechanism of intractable low back pain is unclear. However, intervertebral disc (IVD) degeneration is a primary cause of low back pain, and pain-related mediators, such as interleukin-6 (IL-6), have been correlated with discogenic pain. The objective of this study is to elucidate the mechanism of local IL-6 and IL-6 receptor (IL-6R) expression after IVD injury as well as determine the involvement of IL-6/IL-6 signaling in discogenic pain. To do this, quantitative and immunohistological analyses in a mouse model of IVD injury were performed. Firstly, we measured the local expression levels of IL-6 and IL-6R in IVDs by enzyme-linked immunosorbent assay (ELISA). Secondly, we immunohistochemically confirmed their localization in injured IVDs. Lastly, we evaluated the effects of intradiscal injection of an IL-6 inhibitor by evaluating pain-related protein, calcitonin gene-related peptide (CGRP), expression in dorsal root ganglia (DRG) neurons that innervate IVDs. Injured IVDs showed increased production of IL-6 and IL-6R. IL-6 and IL-6R expression in the injured IVD were predominantly localized in the annulus fibrosus and endplate, and intradiscal injection of the IL-6 inhibitor suppressed CGRP expression in the DRG neurons. These results show that IL-6 and IL-6R expression levels are responsive to IVD injury and that inhibition of IL-6/IL-6R signaling may be a promising analgesic treatment for degenerative disc diseases.
DOI	10.1002/jor.22925
PMID	26010074