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. 2017 May 24;7:2353. doi: 10.1038/s41598-017-02564-9

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© The Author(s) 2017

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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Absence of IPS-1 predisposes towards alarmin release and type-2 inflammation during acute viral infection. (a) Left panel: representative micrograph (40x magnification) of HMGB1 immunostaining. Right panel: Cytoplasmic AEC expression of HMGB1. (b) HMGB1 protein expression in BALF. (c) IL-33 protein expression in BALF. (d) Number of ILC2s in lung at 10 dpi (gated on Lin⁻, CD25⁺, ST2⁺, CD90.2⁺). (e) IL-13 protein expression in BALF. (f) IL-5 protein expression in BALF. (g) Eosinophil number in BALF. Vehicle treated control mice were sacrificed on day 7 of life (i.e. 0 dpi). Experiments were performed twice with 5 to 7 mice per group. Data are mean and the standard error of the mean. *^,**^,***^,****Denotes significance between WT and IPS-1^−/− infected mice. ^#,##,###Denotes significance between infected and vehicle treated IPS-1^−/− mice. Detection limits are denoted by a red dotted line.