Figure 3

IL-36-induced LXR activation inhibits Mtb growth in macrophages. Bacterial growth in IL36R KD cells assessed by [3 H]-uracil uptake (A) and colony forming units (B) after pre-treatment with vehicle, GGPP or 22(S)HC. (C and D) APs mRNA expression in (C) THP-1 macrophages and (D) MDMs upon stimulation with the indicated compounds, (E) upon 24 h Mtb infection in IL-36 signaling blocked THP-1 macrophages and (F) MDM. (G) Intracellular protein levels of hCAP18 (cathelicidin), hBD2 (β-defensin 2) and hBD1 (β-defensin 1) upon 30 h Mtb infection of scramble or IL36R KD THP-1 macrophages with or without LXR inhibitor. Vitamin D and beta actin were used as positive control for AP induction and protein loading control, respectively. (A,B,D and F) Data from one representative experiment of at least three independent experiments are shown. Each dot of MDM represents one donor. MDM and bacterial counts are shown as median ± interquartile range. (C and E) Data pooled from three independent experiments are shown and represented as mean ± SD. (G) Data representative of one experiment of two independent experiments are shown. P values shown as ns p > 0.05; *p ≤ 0.05; **p ≤ 0.01; ***p ≤ 0.001; ****p ≤ 0.0001.