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. 2019 Apr 11;10:1685. doi: 10.1038/s41467-019-09359-8

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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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Fig. 5 — mTOR inhibition in adult macrophages partly mimics phenotype and function of cord blood-derived macrophages. a Enrichment analysis for the top enrichment GO terms from the biological process is shown for rapamycin treated vs. untreated MΦ(IFN-γ) b and for rapamycin treated vs. untreated MΦ(IL-10) macrophages (p < 0.05, FC > 2). c Wikipathway analysis of differentially regulated genes within the cholesterol biosynthesis pathway. MΦ(IL-10) macrophages were compared with rapamycin-treated MΦ(IL-10) macrophages and CBMΦ(IL-10) macrophages. d Wikipathway analysis of differentially regulated genes within the glycolysis and gluconeogenesis pathway. MΦ(IL-10) was compared with rapamycin-treated MΦ(IL-10) macrophages and CBMΦ(IL-10). e ECAR measured under basal conditions and after addition of the indicated drugs in M1–MΦ. Points indicate mean from minimal three to four independent experiments (error bars represent SEM). f ECAR measured under basal conditions and after addition of the indicated drugs in M2–MΦ. Points indicate mean from three to four independent experiments (error bars represent SEM, **p < 0.001, one-way ANOVA). g MΦ(IFN-γ) and MΦ(IL-10) were incubated with E. coli + /− Rapamycin. TNF-α levels were measured by ELISA (N = 3–7; *p < 0.05, blunt-ended bars represent one-way ANOVA, ***p < 0.001). h MΦ(IFN-γ) and MΦ(IL-10) were incubated with E. coli + /− Rapamycin. IL-6 levels were measured by ELISA (N = 3–7; **p < 0.01, blunt-ended bars represent one-way ANOVA, **p < 0.01, ***p < 0.001). i MΦ(IFN-γ) and MΦ(IL-10) were incubated with E. coli + /− Rapamycin. IL-10 levels were measured by ELISA (N = 3–4; *p < 0.05, blunt-ended bars represent one-way ANOVA, *p < 0.05). j MΦ(IFN-γ) and MΦ(IL-10) were incubated with E. coli + /− Rapamycin. IL-1β levels were measured by ELISA (N = 3–7; **p < 0.01, ***p < 0.001, blunt-ended bars represent one-way ANOVA, **p < 0.01, ***p < 0.001; for detailed statistics see supplemental information)