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. 2020 Mar 2;10:3810. doi: 10.1038/s41598-020-60761-5

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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 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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Blocking of TREM-1 by peptide LP17 decreased the expression levels of pro-inflammatory genes during moderate and severe EV-A71 infection. Human primary PBMCs (n = 7) were pre-treated with 100 ng/ml of LP17 or the control sLP17 peptide, before infection with mild, moderate, or severe EV71 isolates at MOI 5. Mock-infected PBMCs were used as negative control. Cells were replenished with fresh media containing respective peptides and harvested at 24 hpi for gene expression and viral load quantifications. (a) Total RNA samples were extracted and gene expression studies were performed via qRT-PCR using 10 ng/µl of RNA. Relative expression levels of genes were calculated by comparing the infected conditions to the respective mock. Bar graphs illustrating the expression levels of genes involved in the TREM-1 pathway. Dotted line indicates the baseline levels from mock. (b) Viral load levels were quantified by qRT-PCR of the VP1 RNA copies. Data are presented as mean ± SD. Statistical analysis was carried out with Wilcoxon matched-pairs signed rank test (*p < 0.05).