Fig. 10From: Extracellular vesicles produced by avian pathogenic Escherichia coli (APEC) activate macrophage proinflammatory response and neutrophil extracellular trap (NET) formation through TLR4 signalingSchematic illustration of EVs interacting with immune cells. Intact EVs are released by APEC CT265 and target the immune cells. Both macrophages and neutrophils sense EVs through TLR4. EVs cause a proinflammatory response in macrophages by activating TLR4 and the NLRP3 inflammasome, triggering the release of proinflammatory cytokines and chemokines. Chemokines promote neutrophil infiltration. Cytosolic EVs also induce macrophage apoptosis via the mitochondria-dependent pathway. EVs induce neutrophils to release NETs via the SAPK/JNK signaling pathway, although the mechanism remains unclearBack to article page