H2S promotes a glycometabolism disorder by disturbing the Th1/Th2 balance during LPS-induced inflammation in the skeletal muscles of chickens

Abstract

Hydrogen sulfide (H2S) is a common environmental pollutant. In humans, H2S enters the body and is transported to different tissues and organs, inducing various types of damage such as chronic inflammatory reactions. Glucose metabolism disorders have been shown to be closely associated with chronic inflammation. The goal of the present study was to investigate the effects and mechanisms of H2S on glycometabolism disorders and chronic inflammatory responses. A chronic inflammation model in the skeletal muscles of chickens was induced using lipopolysaccharide (LPS), after which the animals were exposed to exogenous H2S. Subsequently, the glucose metabolism and the pathways associated with chronic inflammation were analyzed. The pathological analysis showed that significant inflammatory injury to skeletal muscles occurred after animals exposed to H2S. The Th1/Th2 ratio imbalance was exacerbated after exposure to H2S with IFNγ downregulated and IL-1, IL-4, and IL-6 upregulated. In addition, the level of IκBα was suppressed and induced the expression of NF-κB, significantly activating the inflammatory pathway, while the expression of heat shock proteins was elevated. In addition, glucose metabolism factors were analyzed. IRS1 phosphorylation was inhibited in animals exposed to H2S, and the expression of insulin-like growth factor (IGF) signaling pathway-related factors was upregulated to promote insulin resistance, causing glucose metabolism disorders. The results of this study revealed that H2S can trigger changes in the ratio of Th1/Th2 to produce more proinflammatory cytokines that disturb the insulin signaling pathway, causing glycometabolism disorders during the inflammatory response in the skeletal muscles of chickens.