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. 2022 Mar 17;12:4609. doi: 10.1038/s41598-022-08618-x

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© The Author(s) 2022

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Overview of the inflammation-related factors secreted by human macrophages in response to AF16 treatment. THP-1 cells and primary human monocytes were differentiated into M0 macrophages (THP-1 derived M0, grey columns and primary mono-derived M0, white columns, respectively) and treated with 1 µg/ml and 100 µg/ml AF16 or 1 µM betamethasone (BM), or into M1 and M2 macrophages (M1, M2 respectively). Other M0 cells were left untreated (M0 UTR). The levels of IL1β (a), IL13 (c), IP10 (d) and TNFα (g) were upregulated in M0-T and M0-P cells after AF16 treatment, while IL8 (b), MIP1α (f), MIP1β (e) were upregulated in M0-T and downregulated in M0-P by AF16. Levels of MIP1α in THP-1 derived M0 and M1 cells were replaced by upper limit of quantification (marked with x). Values are shown in pg/ml on a logarithmic scale.