Extended Data Fig. 4: β-glucan-driven granulopoiesis is dependent on type I IFN signalling.
From: β-Glucan reprograms neutrophils to promote disease tolerance against influenza A virus
(a-e) Kinetics of LKS/progenitors in the BM of β-glucan treated mice. Frequency of LKS (a), MPP (b), GMP (c), GP (d), cMoP (e) in the BM of β-glucan treated mice (n = 4, data pooled from two individual experiments). (f-h) Dectin-1-/- mice were treated with β-glucan. Total cell number of LKS (f), GMP (g) and neutrophils (h) at day 4 (n = 5). C57BL/6 (WT and Il1r-/-) mice were treated with β-glucan. Frequency of neutrophils in the BM (i); and lungs (j) of β-glucan treated mice at day 4. (k-r) WT and Ifnar1-/- mice were treated with β-glucan. Frequency and total cell counts of LKS (k); MPP (l); GMP (m); and GP (n) in the BM at day 4 post-glucan treatment (n = 5). Frequency of neutrophils in the BM (o, p) and lungs (q, r) at day 4 post β-glucan treatment (n = 5, data pooled from two individual experiments). (s) Chimerism was confirmed via flow cytometry. (t-v) Mice were treated with PolyI:C (i.p.). Frequency (u) and total cell counts (v) of neutrophils in the lungs post-PolyI:C (n = 4). (w, x) Mice were infected with IAV (lethal dose) 6 days post-PolyI:C (w), survival was monitored overtime (x) (n = 10). Data represented as mean ± SEM. Data were analyzed using one-way ANOVA followed by Sidak’s multiple comparisons tests (a-e, u, v) or two-way ANOVA followed by Sidak’s multiple comparisons tests (f-r). Survival was monitored by a log-rank test (x). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001. Illustrations in t and w created using BioRender.com.
