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

Abstract

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.