TLR4 induced Wnt3a-Dvl3 restrains the intensity of inflammation and protects against endotoxin-driven organ failure through GSK3β/β-catenin signaling.

•TLR4 activation enhances the expression of Wnt3a and Dvl3 in innate immune cells.•Wnt3a-Dvl3 reduces pro-inflammatory cytokine production via β-catenin/NF-κB pathway.•Wnt3a restrains inflammation intensity and protects mice from lethal endotoxemia.•Wnt3a signaling could be a target to manipulate the intensity of inflammation.