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. 2020 Jan 21;10:777. doi: 10.1038/s41598-019-57275-0

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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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The immune response of macrophage from wild-type (WT) and FcGRIIb−/− after stimulated in vitro with phosphate buffer solution control (PBS) or LPS with and without purified (1→3)-β-D-glucan (BG) after 24 h incubation was demonstrated (A). Quantitative flow-cytometric analysis of macrophage from WT and FcGRIIb−/− mice after LPS-stimulation with and without BG following by cell starvation (see methods) to determine necrotic cells (propidium iodide; PI +ve) (B), early apoptosis cells (Annexin V +ve, PI −ve) (C), late apoptosis cells (Annexin V +ve, PI +ve) (D) were demonstrated. In addition, other parameters of macrophage injury from these activations in TNF-related apoptosis-inducing ligand (TRAIL) (E), copy numbers of mitochondria DNA (mtDNA) (F), reactive oxygen species production as detected by dihydroethidium (DHE) (G) and total cell energy with ATP luminescence intensity (H) were indicated (independent triplicate experiments were performed). *p < 0.05; ^#p < 0.05 vs. same mouse strain in other experimental groups.