H2S exposure induces cell death in the broiler thymus via the ROS-initiated JNK/MST1/FOXO1 pathway

Hydrogen sulfide (H2S) is a common toxic gas in chicken houses that endangers the health of poultry. Harbin has a cold climate in winter, and the conflict between heat preservation and ventilation in poultry houses is obvious. In this study, we investigated the H2S content in chicken houses during winter in Harbin and found that the H2S concentration exceeded the national standard in individual chicken houses. Then, a model of H2S exposure was established in an environmental simulation chamber. We also developed a NaHS exposure model of chicken peripheral blood lymphocytes in vitro. Proteomics analysis was used to reveal the toxicology of thymus injury in broilers, the FOXO signaling pathway was determined to be significantly enriched, ROS bursts and JNK/MST1/ FOXO1 pathway activation induced by H2S exposure were detected, and ROS played an important switch role in the JNK/MST1/FOXO1 pathway. In addition, H2S exposure-induced thymus cell death involved immune dysregulation. Overall, the present study adds data for H2S contents in chicken houses, provides new findings for the mechanism of H2S poisoning and reveals a new regulatory pathway in immune injury.

Automated summary

The study found that hydrogen sulfide (H2S) levels exceeded national standards in chicken houses in Harbin, posing a hazard to poultry health. By establishing H2S exposure and NaHS exposure models, the mechanisms of H2S toxicity on the immune system of chickens were revealed.