Hydrogen sulfide exposure triggers chicken trachea inflammatory injury through oxidative stress-mediated FOS/IL8 signaling.

Abstract

Hydrogen sulfide (H2S) is well known to cause irritation and damage to airway following inhalation, but the mechanism by which H2S contributes to airway toxicity is unclear. In order to assess the respiratory toxicity of H2S inhalation in chicken trachea, we investigated the change of oxidative stress parameters, tracheal tissue structure and transcriptome profiles of chicken trachea exposed to H2S for 42 days. The results showed H2S exposure induced oxidative stress and inflammation in trachea. The ultrastructural analysis revealed loss of cilia and accumulation of mucus in tracheal epithelium. Differentially expressed genes (DEGs) analysis indicated 454 genes were significantly changed, including 136 genes upregulated and 318 genes downregulated. Gene ontology and KEGG analysis showed many genes involved in response to oxidative stress, inflammatory and immune response, which might contribute to H2S-induced tracheal inflammatory injury. Among those genes, N-acetyl-L-cysteine (NAC) treatment blocked the H2S-triggered expression of FOS and IL8. Silencing FOS by siRNA inhibited H2S-induced expression of IL8. Taken together, we concluded that H2S induced oxidative stress leads to tracheal inflammation through FOS/IL8 signaling, leading to excessive mucus secretion and absence of cilia. These results provide new insights for unveiling the biological effects of H2S in vivo and in vitro.