The release of FB1-induced heterophil extracellular traps in chicken is dependent on autophagy and glycolysis

Fumonisin B1 (FB1), a worldwide con-taminating mycotoxin produced by Fusarium, poses a great threat to the poultry industry. It was reported that extracellular traps could be induced by FB1 effi-ciently in chickens. However, the relevance of autophagy and glycolysis in FB1-triggered heterophil extracellular trap (HET) formation is unclear. In this study, immu-nostaining revealed that FB1-induced HETs structures were composed of DNA coated with histones H3, and elastase, and that heterophils underwent LC3B-related autophagosome formation assembly driven by FB1. Western blotting showed that FB1 downregulated the phosphorylated phosphoinositide 3-kinase3-kinase (PI3K)/protein kinase B (AKT)/mechanistic target of rapamycin complex 1 (mTORC1) axis and raised the AMP-activated kinase a (AMPKa) activation protein. Furthermore, rapamycin-and 3-Methyladenine (3 -MA)-treatments modulated FB1-triggered HET forma-tion according to the pharmacological analysis. Further studies on energy metabolism showed that glucose/lac-tate transport and glycolysis inhibitors abated FB1- induced HETs. These results showed that FB1-induced HET formation might interact with the autophagy pro-cess and relied on glucose/monocarboxylic acid trans-porter 1 (MCT1) and glycolysis, reflecting chicken's early innate immune responses against FB1 intake.