Deoxynivalenol-induced pyroptosis and autophagy inhibition collectively promote inflammatory injury in the glandular stomach of chicken embryos

Abstract

Glandular stomach plays a crucial role in the digestive system and overall physiological functions of chickens. Mycotoxins, including deoxynivalenol (DON), in contaminated feed damage the immune and digestive systems of chickens and hinder their growth. However, the mechanism underlying DON toxicity on glandular stomach inflammation remains unclear. This study found that DON induced inflammation and injury in the glandular stomach of chicken embryos by regulating pyroptosis and autophagy. DON stimulated proinflammatory factor release, activated NLRP3 inflammasome and its downstream elements, increased caspase-3 and GSDME expression to mediate pyroptosis and injury, and inhibited autophagy in glandular stomach by decreasing ATG5, ATG7, and Beclin-1 expressions and increasing mTOR expression. Besides, DON reduced LC3-II/LC3-I ratio and elevated p62 expression. These results confirmed the association between DON-induced pyroptosis and autophagy inhibition, providing key evidence for understanding DON toxicity and mitigating DON contamination in poultry farming; nevertheless, the underlying mechanism must be further elucidated.

Keywords

• Deoxynivalenol
• glandular stomach
• chicken embryos
• pyroptosis
• autophagy