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. 2020 Oct 14;10:17178. doi: 10.1038/s41598-020-73989-y

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© The Author(s) 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 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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IL-26 displays extracellular antimycobacterial activity against Mtb H37Rv and improves intracellular killing of Mtb H37Rv pBEN::mCherry in THP1 macrophages. Growth of MtbH37Rv (a) treated with increasing concentrations of IL-26 or LL37 was analyzed using the resazurin assay (n = 3–6). (b) Scanning electron microscopy of untreated Mtb (left picture), IL-26-treated Mtb (middle picture) and LL37-treated Mtb (right picture). (c) Binding of IL-26 to mycobacterial ManLAM was investigated using microscale thermophoresis (MST). The percentages of bound fractions of LAM from Mtb H37Rv to different IL-26, IL-22 and LL37 concentrations are displayed graphically. (d) CFUs from infected THP1 macrophages after treatment with IL-26 (n = 3). Data are presented as mean ± SEM. Statistical analysis was done using Wilcoxon matched pairs signed rank test (* equals p < 0.05, ** equals p < 0.01).