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. 2018 Jan 24;8:1520. doi: 10.1038/s41598-018-19476-x

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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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rIL-36γ drives expression of cholesterol-converting enzymes and endogenous LXR ligands. (A and B) mRNA expression of CH25H, CYP27A1, CYP46A1 and CYP7A1 in (A) THP-1 macrophages and MDM upon 4 h of stimulation with various doses of rIL-36γ and (B) 12 h Mtb-infection with or without blocking IL-36R signaling. (C and D) Concentrations of intracellular 25HC or 27HC in cell lysates of THP-1 macrophages (C) upon stimulation with rIL-36γ or rIL-1β or (D) after Mtb infection. (E) LXR luciferase activity in THP-1 macrophages treated with DMSO or 500 nM of 25HC, 27HC or GW3965 for 8 h. (A–E) Data from THP-1 macrophages are pooled from three independent experiments and shown as mean ± SD. MDM data are from one representative experiment of three independent experiments, median ± interquartile range is shown and each dot of MDM represents one donor. P values shown as ns p > 0.05; *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001.