Atmospheric H2S triggers immune damage by activating the TLR-7/MyD88/NF-κB pathway and NLRP3 inflammasome in broiler thymus.

Atmospheric hydrogen sulfide (H2S) is a highly toxic air pollutant that has a negative effect on human health and animal welfare. The immunotoxicity of H2S has been explored previously, but its mechanism still needs to be clarified, especially in chickens. To further evaluate the immunotoxicity of H2S, 1-day-old broilers were recruited and exposed to atmospheric H2S for 42 days of age. Our results showed that H2S 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 H2S 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 H2S toxicity in chicken thymus. We measured 172 differently expression genes (DEGs) after H2S 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 H2S significantly increased IL-1β, IL-4 and IL-10 levels, whereas it downregulated IL-12 and IFN-γ. This study confirmed that H2S triggered the thymus inflammatory response and caused a Th1/Th2 imbalance. Moreover, our results demonstrated that H2S triggered the TLR-7/MyD88/NF-κB pathway to promote NLRP3 inflammasome activation. In conclusion, atmospheric H2S 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 H2S.