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. 2018 Apr 10;8:5723. doi: 10.1038/s41598-018-24152-1

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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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Loss of KLF4 decreases pneumococci-induced proinflammatory cytokine response and up-regulates antiinflammatory IL-10 secretion in BMMs. BMMs derived from C57BL/6 LyzMcre^−/−/Klf4^loxP/loxP (KLF4^+/+) and C57BL/6 LyzMcre^+/+/Klf4^loxP/loxP (KLF4^−/−) mice were stimulated with 10⁶ CFU/ml S. pneumoniae D39 for 15 h. Supernatants were collected and IL-1β (a), TNFα (b), IL-6 (c) and IL-10 (d) ELISAs were performed. Data represents mean ± SEM of 6 independent experiments. Differences were indicated as follows: *p < 0.05; **p < 0.01; ***p < 0.001.