H₂S induces Th1/Th2 imbalance with triggered NF-κB pathway to exacerbate LPS-induce chicken pneumonia response

H₂S is one of the air pollutants, which can cause multiple organ damage to the body. H₂S exposure will directly damage respiratory system and cause inflammatory reaction. In this experiment, the effect of H₂S on LPS-induce chicken pneumonia is explored from the Th1/Th2 balance and the NF-κB pathway. 42-day-old broilers was selected as research object, exposed to exogenous H₂S, received an intraperitoneal injection of LPS to establish inflammatory model on forty-second days. We carry out qRT-PCR and Western blot to detect the expression of cytokines secreted by Th1/Th2, PPAR-γ/HO-1 genes, NF-κB pathway genes and the downstream genes COX-2 and iNOS. We found the expression of IL-4, IL-6, TNF-α and IL-1β increased and that of IFN-γ decreased, which indicating the immune imbalance of Th1/Th2 was occurred and the level of PPAR-γ/HO-1 was significantly suppressed. In addition, the activation of I-κB-β and NF-κB genes with the degradation of I-κB-α indicated that NF-κB pathway has been activated, which accompanied with COX-2, PGE and iNOS increasing. These results suggested that H₂S exposure can lead to Th1/Th2 immune imbalance, repress the anti-inflammatory effect of PPAR-γ/HO-1, and then activate NF-κB pathway-related genes and the downstream genes to aggravate pneumonia induced by LPS.