Atmospheric HS triggers immune damage by activating the TLR-7/MyD88/NF-κB pathway and NLRP3 inflammasome in broiler thymus.

Atmospheric hydrogen sulfide (HS) is a highly toxic air pollutant that has a negative effect on human health and animal welfare. The immunotoxicity of HS has been explored previously, but its mechanism still needs to be clarified, especially in chickens. To further evaluate the immunotoxicity of HS, 1-day-old broilers were recruited and exposed to atmospheric HS for 42 days of age. Our results showed that HS significantly reduced the thymus index and the CD4 and CD8 T-lymphocyte numbers and that it also changed the CD4/CD8 ratio. The morphological analysis showed that HS incrassated the medulla and generated inflammatory infiltration. In addition, it caused the mitochondria to swell and the chromatin to condense, and destroyed nuclear structures were observed. We also conducted bioinformation and transcriptomic analyses to delve the mechanism of HS toxicity in chicken thymus. We measured 172 differently expression genes (DEGs) after HS exposure and further filtrated the DEGs that are related to inflammation and cell death that play a critical role in immune function. We concluded that HS significantly increased IL-1β, IL-4 and IL-10 levels, whereas it downregulated IL-12 and IFN-γ. This study confirmed that HS triggered the thymus inflammatory response and caused a Th1/Th2 imbalance. Moreover, our results demonstrated that HS triggered the TLR-7/MyD88/NF-κB pathway to promote NLRP3 inflammasome activation. In conclusion, atmospheric HS actives the TLR-7/MyD88/NF-κB pathway and the NLRP3 inflammasome to promote an inflammatory response, which then causes tissues damage in broiler thymus. These results provide new insights for unveiling the immunotoxic effects of HS.