Fig. 1.

Myeloid POH1 deficiency accelerates inflammation in vivo. a Poh1^+/+ (n = 14), Poh1^Δ/+ (n = 14) and Poh1^Δ/Δ (n = 15) mice were intraperitoneally (i.p.) injected with LPS (40 mg/kg). Survival was monitored for up to 60 h, ***p < 0.001 (asymmetrical log-rank Mantel–Cox survival test). b–d ELISA quantification of the (b) IL-1β, (c) IL-6 and (d) TNFα levels in the serum of Poh1^Δ/+ and Poh1^Δ/Δ mice upon LPS challenge (n = 9 per group). e Lungs of Poh1^Δ/+ and Poh1^Δ/Δ mice were harvested 6 h post-LPS injection, and then the transcriptional levels of IL-1β, IL-6 and TNFα were measured by RT-PCR (n = 9 per group). f-j Poh1^Δ/+ and Poh1^Δ/Δ mice were i.p. injected with (n = 8–9 per group) or without (n = 6 per group) 40 mg/kg of alum crystals, and then peritoneal fluids were elicited 12 h after the treatment and subjected to analysis of f IL-1β, g IL-6 and h TNFα by ELISA; absolute numbers of i CD11b⁺ Ly6G⁺ neutrophils or j CD11b⁺ Ly6C⁺ monocytes recruited to the peritoneum were measured. Data are pooled from a three or b-j two independent experiments (mean ± s.e.m. in b-h; mean ± s.d. in i, j), *p < 0.05, **p < 0.01 (two-tailed Student’s t-test)