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. 2017 May 8;7:1578. doi: 10.1038/s41598-017-01822-0

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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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Selected TKIs inhibit RIPK2-mediated cytokine responses in macrophages induced by bacterial cell wall components, but not endotoxin. Levels of Cxcl1 released from WT (left panel) or RIPK2^−/− (right panel) bone marrow-derived macrophages (BMDMs) after stimulation with the Nod1 ligand FK565 (10 μg/mL) for 48 h and pre-incubated for 1 h with 0.2, 1 or 5 μM gefitinib or SB203580 (A) n = 4–12. Time course of FK565-stimulated Cxcl1 secretion in BMDMs (B) n = 4–12. Levels of Cxcl1 released from WT (left panel) or RIPK2^−/− (right panel) BMDMs after stimulation with the Tlr4 ligand LPS (0.5 μg/mL) for 48 h and pre-incubated for 1 h with 0.2, 1 or 5 μM gefitinib or SB203580 (C) n = 4–12. Time course of LPS-stimulated Cxcl1 secretion in BMDMs (D) n = 4–12. Values are mean ± SEM. Different letters assigned to each condition (a, b, c) denote statistical differences between groups (p < 0.05).