The release of FB(1)-induced heterophil extracellular traps in chicken is dependent on autophagy and glycolysis

Fumonisin B(1) (FB(1)), a worldwide contaminating mycotoxin produced by Fusarium, poses a great threat to the poultry industry. It was reported that extracellular traps could be induced by FB(1) efficiently in chickens. However, the relevance of autophagy and glycolysis in FB(1)-triggered heterophil extracellular trap (HET) formation is unclear. In this study, immunostaining revealed that FB(1)-induced HETs structures were composed of DNA coated with histones H3, and elastase, and that heterophils underwent LC3B-related autophagosome formation assembly driven by FB(1). Western blotting showed that FB(1) 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 α (AMPKα) activation protein. Furthermore, rapamycin- and 3-Methyladenine (3-MA)-treatments modulated FB(1)-triggered HET formation according to the pharmacological analysis. Further studies on energy metabolism showed that glucose/lactate transport and glycolysis inhibitors abated FB(1)-induced HETs. These results showed that FB(1)-induced HET formation might interact with the autophagy process and relied on glucose/monocarboxylic acid transporter 1 (MCT1) and glycolysis, reflecting chicken's early innate immune responses against FB(1) intake.