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. Author manuscript; available in PMC: 2021 Jun 3.
Published in final edited form as: Nat Metab. 2021 Apr 12;3(4):513–522. doi: 10.1038/s42255-021-00366-y

Extended Data Fig. 8 |. Colchicine-induced GDF15 inhibits pro-IL-1β expression by activating the immuno-inhibitory signal of SHP-1 in primary neutrophils.

Extended Data Fig. 8 |

Ex vivo activation of neutrophils evaluated by the levels of (a–b) pro-IL-1β induction or (c–d) phosphorylated SHP-1. Cells were pre-incubated with plasma from the indicated mice and then activated with PMA. a, Induction of GDF15 specifically in hepatocytes was required for the anti-inflammatory activity of post-colchicine plasma, as assayed by pro-IL-1β induction. GalNAc-siLuc, hepatocyte-specific sirNA against luciferase. GalNAc-siGDF15, hepatocyte-specific sirNA against GDF15. b, The anti-inflammatory activity of post-colchicine plasma was blocked by two different clones of antibodies (#2 and #3) against GDF15. ctr, control antibody. veh plasma, plasma from vehicle-treated mice. Colc plasma, plasma from colchicine-treated mice. c, GDF15 neutralization by two clones of anti-GDF15 antibodies (#2 and #3) blocked plasma activity on stabilizing SHP-1 activation. d, Expression of colchicine-induced GDF15 specifically in hepatocytes was required for activating SHP-1. 3 Biological replicates.