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Interleukin-27 controls basal pain threshold in physiological and pathological conditions

発表形態:
原著論文
主要業績:
主要業績
単著・共著:
共著
発表年月:
2018年07月
DOI:
https://doi.org/10.1038/s41598-018-29398-3
会議属性:
国際会議(国内開催を含む)
査読:
有り
リンク情報:

日本語フィールド

著者:
Tomoko Sasaguri Toru Taguchi Yuzo Murata Kimiko Kobayashi Sayaka Iizasa Ei’ichi Iizasa Makoto Tsuda Naomi Hirakawa Hiromitsu Hara Hiroki Yoshida Toshiharu Yasaka
題名:
Interleukin-27 controls basal pain threshold in physiological and pathological conditions
発表情報:
Tomoko Sasaguri^D Toru Taguchi Yuzo Murata Kimiko Kobayashi Sayaka Iizasa Ei’ichi Iizasa Makoto Tsuda Naomi Hirakawa Hiromitsu Hara Hiroki Yoshida Toshiharu Yasaka 巻: 8 ページ: Article number: 11022 (2018)
キーワード:
概要:
抄録:
Numerous studies have shown that pain sensation is affected by various immune molecules, such as cytokines, in tissues comprising the sensory pathway. Specifically, it has been shown that interleukin (IL)-17 promotes pain behaviour, but IL-10 suppresses it. IL-27 has been reported to have an anti-inflammatory effect through regulation of T cell differentiation, resulting in reduced IL-17 and induction of IL-10. Thus, we hypothesised that IL-27 would have some regulatory role in pain sensation. Here, we provide evidence that endogenous IL-27 constitutively controls thresholds for thermal and mechanical sensation in physiological and pathological conditions. Mice lacking IL-27 or its receptor WSX-1 spontaneously showed chronic pain-like hypersensitivity. Reconstitution of IL-27 in IL-27-deficient mice reversed thermal and mechanical hypersensitive behaviours. Thus, unlike many other cytokines induced by inflammatory events, IL-27 appears to be constitutively produced and to control pain sensation. Furthermore, mice lacking IL-27/WSX-1 signalling showed additional hypersensitivity when subjected to inflammatory or neuropathic pain models. Our results suggest that the mechanisms underlying hypersensitive behaviours caused by the ablation of IL-27/WSX-1 signalling are different from those underlying established chronic pain models. This novel pain control mechanism mediated by IL-27 might indicate a new mechanism for the chronic pain hypersensitivity.

英語フィールド

Author:
Tomoko Sasaguri Toru Taguchi Yuzo Murata Kimiko Kobayashi Sayaka Iizasa Ei’ichi Iizasa Makoto Tsuda Naomi Hirakawa Hiromitsu Hara Hiroki Yoshida Toshiharu Yasaka
Title:
Interleukin-27 controls basal pain threshold in physiological and pathological conditions
Announcement information:
Sci Rep Vol: 8 Page: Article number: 11022 (2018)
An abstract:
Numerous studies have shown that pain sensation is affected by various immune molecules, such as cytokines, in tissues comprising the sensory pathway. Specifically, it has been shown that interleukin (IL)-17 promotes pain behaviour, but IL-10 suppresses it. IL-27 has been reported to have an anti-inflammatory effect through regulation of T cell differentiation, resulting in reduced IL-17 and induction of IL-10. Thus, we hypothesised that IL-27 would have some regulatory role in pain sensation. Here, we provide evidence that endogenous IL-27 constitutively controls thresholds for thermal and mechanical sensation in physiological and pathological conditions. Mice lacking IL-27 or its receptor WSX-1 spontaneously showed chronic pain-like hypersensitivity. Reconstitution of IL-27 in IL-27-deficient mice reversed thermal and mechanical hypersensitive behaviours. Thus, unlike many other cytokines induced by inflammatory events, IL-27 appears to be constitutively produced and to control pain sensation. Furthermore, mice lacking IL-27/WSX-1 signalling showed additional hypersensitivity when subjected to inflammatory or neuropathic pain models. Our results suggest that the mechanisms underlying hypersensitive behaviours caused by the ablation of IL-27/WSX-1 signalling are different from those underlying established chronic pain models. This novel pain control mechanism mediated by IL-27 might indicate a new mechanism for the chronic pain hypersensitivity.


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