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. 2018 Oct 17;8:15331. doi: 10.1038/s41598-018-32853-w

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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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Imatinib lowers pro-inflammatory activation in human monocytes, but hyperglycemia alters their responsiveness. (a,b) Fold change gene expression of TNFα, MCP-1 and CD163 in human M0- (a) or M1-monocytes (b) treated with 1 μM of imatinib (M0 + IM or M1 + IM, open bars) compared to non-treated M0- or M1-monocytes (M0 or M1, closed bar) from healthy controls (He, n = 6), adequately controlled diabetics (aDM, n = 5) and inadequately controlled diabetics (iaDM, n = 5). (c) Fold change of gene expression of TNFα, MCP-1 and CD163 with increasing doses of imatinib (1, 2.5, 5 μM) in inadequately controlled diabetics (n = 3). Data expressed as mean ± SEM, *p < 0.05, **p < 0.01.