Interleukin-27 controls basal pain threshold in physiological and pathological conditions
Autor: | Naomi Hirakawa, Hiromitsu Hara, Toshiharu Yasaka, Yuzo Murata, Tomoko Sasaguri, Ei’ichi Iizasa, Kimiko Kobayashi, Makoto Tsuda, Sayaka Iizasa, Toru Taguchi, Hiroki Yoshida |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
Male
Pain Threshold 0301 basic medicine Interleukin-27 Adolescent lcsh:Medicine Article Nociceptive Pain Minor Histocompatibility Antigens 03 medical and health sciences Threshold of pain Sensation medicine Animals Humans Receptors Cytokine Interleukin 27 Child lcsh:Science Multidisciplinary Behavior Animal business.industry lcsh:R Chronic pain Nociceptors Interleukin Receptors Interleukin medicine.disease Immunohistochemistry Electrophysiology 030104 developmental biology Nociception Immunology Neuropathic pain Nociceptor lcsh:Q Capsaicin business |
Zdroj: | Scientific Reports, Vol 8, Iss 1, Pp 1-13 (2018) Scientific Reports |
ISSN: | 2045-2322 |
DOI: | 10.1038/s41598-018-29398-3 |
Popis: | 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. |
Databáze: | OpenAIRE |
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