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. 2018 Jul 23;8:11022. doi: 10.1038/s41598-018-29398-3

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Mice lacking IL-27/WSX-1 signalling still develop mechanical hypersensitivity after inflammation and peripheral nerve injury. Mice were subjected to the (a–c) inflammatory or (d–g) neuropathic pain model. Fifty percent paw withdrawal threshold before and after (a) CFA injection or (d) spinal nerve injury. (b,e) The percent change in paw withdrawal threshold calculated from a and d, respectively. Each value after CFA injection or nerve injury was normalised by the control value (pre) in each mouse. (c) Hind paw weight, as a measure of oedema, in mice 14 days after i.pl. CFA injection. (f) Representative immunofluorescence labelling for Iba1 (green) with nuclear staining with TO-PRO-3 (blue) in a transverse section of the dorsal horns from the L4 segment of WT, WSX-1^−/−, EBI3^−/−, and p28^−/− mice 7 days after spinal nerve injury. (g) Number of Iba1-positive cells in the ipsilateral or contralateral dorsal horn of L4 spinal segments dissected from WT, WSX-1^−/−, EBI3^−/−, and p28^−/− mice 7 days after spinal nerve injury. n = 5 animals/group. All data are expressed as means ± SEM.