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. 2019 May 22;9:7677. doi: 10.1038/s41598-019-44181-8

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© The Author(s) 2019

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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(a) LPS responsiveness is only present in CD11b^HI macrophages as early as E13. Macrophage populations from E13 mouse lung, yolk sac, and liver were sorted, isolated, and stimulated with LPS. Only F4/80^HI macrophages could be isolated from E13 lung and yolk sac. LPS did not increase cytokine expression or release from E13 F4/80^HI macrophages (+/− s.e.m.; *P < 0.05, n = 3–7). (b) F4/80^HI macrophages in E15 mouse brains have a partial response to LPS. The majority of macrophages in E15 brain were F4/80^HI, and LPS treatment did not increase IL-1β release or mRNA expression (+/− s.e.m.; n = 6–7). Intracellular staining and FACS did demonstrate increased TNF expression in F4/80^HI macrophages from E15 brain, but only minimal pro-IL-1β expression (representative data from three independent experiments shown).