Fig. 4: β-Glucan increases granulopoiesis and is independent of IL-1 signaling.
From: β-Glucan reprograms neutrophils to promote disease tolerance against influenza A virus
a, Mice were treated with β-glucan, HSCs or progenitors and immune cells were assessed in the BM at days 2, 4 and 7 post-β-glucan treatment. b–e, Expansion of LKSs (b), MPPs (c), GMPs (d) and GPs (e) in the BM (n = 5). f–h, Representative FACS plots (f), frequency (g) and total cell counts of neutrophils (h) in the BM (n = 5). i, C57BL/6 (WT and Il1r−/−) mice were treated with β-glucan. j–l, Neutrophils in the BM (j), blood (k) and lungs (l) at day 4 post-β-glucan treatment (n = 5). Data are pooled from two individual experiments. m, Survival of Il1r−/− or WT mice after β-glucan treatment following IAV infection (lethal dose) at day 7 (n = 10). Data are represented as mean ± s.e.m. Data were analyzed using one-way ANOVA followed by Tukey’s multiple-comparison test (b–e, g and h) or two-way ANOVA followed by Šidák’s multiple-comparison tests (j–l). Survival was monitored by a log(rank) test (m). *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Illustrations in a and i created using BioRender.com.
