a, b, PGE2 measured in BALF of indicated mouse strains 4 weeks post infection (p.i.) (n = 5) (a) and WT or Il1α,Il1β−/− BMDM infected for 40 h (m.o.i. = 5) or in the presence or absence of recombinant murine IFN-β (rmIFNβ; b). c, PGE2 in supernatants of MDM from 22 healthy donors, 24 h after Mtb infection (m.o.i. = 5) in the presence or absence of rhIFN-β (Wilcoxon matched pairs test). d, IfnbmRNA expression and IFN-β protein in lungs of Mtb-infected WT or Il1r1−/− mice at indicated time points. AU, arbitrary units (n = 9). e, f, IFN-βprotein in supernatants of WT or Il1α,Il1β−/− BMDM infected for 40 h (e) or WT BMDM in the presence or absence of rmIL-1α or IL-1β (f). g, IFN-β protein concentration in supernatants WT BMDM (40 h p.i. Mtb) treated with increasing concentrations of PGE2. h, IFN-β protein in supernatants of MDM from 7 healthy donors, 24 h after Mtb infection with or without PGE2 (Wilcoxon matched pairs test). i, c.f.u. at indicated time points of Mtb-infected (m.o.i. = 5) WT BMDM cultures treated with anti-IFNAR1 monoclonal antibody, rmIL-1α or Il-1β, rmIFN-β or PGE2. j, c.f.u. after 5 days of Mtb infection (m.o.i. = 5) of Il1r1−/− BMDM treated with anti-mIFNAR1 mAb or PGE2. k, Survival of WT, Il1r1−/−, Ifnar1−/− or Il1r1,Ifnar1−/− double-deficient animals after Mtb infection (n = 5, Mantel–Cox test). Data shown are representative of two (a, b, d–g, i, k) or three (j) independent experiments. *P ≤ 0.05; **P < 0.005; ***P < 0.0005; compared as indicated in figure by lines or to WT control groups. Error bars denote s.d. (Mann–Whitney test).