H2S induces Th1/Th2 imbalance with triggered NF-κB pathway to exacerbate LPS-induce chicken pneumonia response. (October 2018)

• Record Type: Journal Article
• Authors: Wang, Wei; Chen, Menghao; Jin, Xi; Li, Xiaojing; Yang, Zijiang; Lin, Hongjin; Xu, Shiwen
• Is Part Of: Chemosphere. Volume 208(2018)
• Page Start: 241
• Page End: 246
• Publication Date: 2018-10
• Subjects: H2S -- Chicken lungs -- NF-κB-pathway -- Inflammation; Pollution -- Periodicals; Pollution -- Physiological effect -- Periodicals; Environmental sciences -- Periodicals; Atmospheric chemistry -- Periodicals; 551.511
• DOI: 10.1016/j.chemosphere.2018.05.152
• Languages: English
• ISSNs: 0045-6535

Abstract

Abstract: H2 S is one of the air pollutants, which can cause multiple organ damage to the body. H2 S exposure will directly damage respiratory system and cause inflammatory reaction. In this experiment, the effect of H2 S 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 H2 S, 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 H2 S 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. Highlights: Exposure of H2 S aggravates LPS-induce inflammatory damage. LPS leads to Th1/Th2 imbalance, this imbalance is enhanced by H2 S exposed. The NFκB pathway mediates the inflammation trigged by LPS and performs more significant in LPS infected after H2 S exposed. The role of PPARγ/HO-1 loses predominance in LPS-induce inflammation and more worse in LPS infected after H2 S exposed.