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. 2020 Sep 16;11:4678. doi: 10.1038/s41467-020-18276-0

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© This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply 2020

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 — a Top functions enriched in the inflammatory response demonstrating inhibition of immune-cell activation in DFUs. b Prediction of estimated proportions of a subset of leukocytes (macrophages and granulocytes) in oral, skin, and DFUs based on gene expression demonstrates decreased macrophage activation and neutrophil recruitment with increased eosinophils in DFUs. c Subset of genes involved in activation of phagocytes showing downregulation of several genes in DFUs (n = 8 biologically independent samples). d Representative pictures of oral and skin day 3 wounds and DFUs show basal keratin marker K5, macrophage marker, and neutrophil marker MPO. Quantification of n = 5 biologically independent samples demonstrates decreased macrophage activation (**P = 0.0038, ****P ≤ 0.0001) and neutrophils (**P = 0.0048, ****P ≤ 0.0001) in DFUs compared to oral and skin wounds. Data presented as mean ± SD (two-tailed unpaired Student’s t-test). Scale bar = 100 µm.