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. 2022 Jan 18;132(2):e144983. doi: 10.1172/JCI144983

Figure 1. Anakinra induces autophagy and limits inflammation in the absence of IL-1R1.

Figure 1

(A–D) LC3 staining of RAW 264.7 cells treated with 50 μM rapamycin, 10 μg/mL anakinra, or a truncated form (Anakinra*) (A and B); exposed to A. fumigatus conidia and treated with anakinra with and without 100 nM bafilomycin for 4 hours (C and D). (E and F) LC3 staining of alveolar macrophages purified from Il1r1–/– naive mice exposed to A. fumigatus conidia and treated with anakinra and/or bafilomycin as above. (B, D, and F) Mean percentage of LC3 puncta/cells (n = 4–22). Data represent the mean ± SEM of 1 representative out of 3 (A–D) or 2 (E and F) independent experiments. DAPI was used to detect nuclei. (G–I) Il1r1–/– mice were infected (i.n.) with live A. fumigatus conidia, treated with 10 mg/kg anakinra (i.p.) as described in Methods, and assessed for immunoblotting of LC3b and p62 (G), cytokine production (ELISA) in lung homogenates (H), and lung histology [periodic acid-Schiff (PAS) staining] (I) at 7 days after infection. Scale bar: 200 μm. (G and I) A representative experiment is shown; (H) data represent 3 independent experiments. Each independent in vivo experiment includes 6–8 mice per group pooled before analysis. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001, treated versus untreated (None) cells. One-way ANOVA, Bonferroni post hoc test.