Ammonia induces Treg/Th1 imbalance with triggered NF-κB pathway leading to chicken respiratory inflammation response.

Ammonia (NH3) is a severe air pollutant and a component of haze (PM2.5). The respiratory tract is the first route of exogenous ammonia's entry into the human and animal body. Many studies have suggested that exposure to NH3 is associated with a higher risk of respiratory tract tracheitis; however, the underlying mechanism remains unclear. In this study, chicken tracheas were used as a model to investigate toxic effects and genetic changes induced by NH3 exposure, as evaluated by scanning electron microscopy (SEM) and bioinformatic analyses. The transcript analysis illustrated that NH3 exposure caused immune disorders, which play key roles in regulating inflammatory responses from NH3 exposure. Therefore, we carried out Real-time quantitative PCR (RT-PCR) and Western Blot analyses to detect the immune response genes; Treg/Th1, Th2 and Th17 secretions were found that led to inflammatory responses. Next, we also detected the NF-κB pathway and downstream genes, accompanied by cytochromes P450 (CYPs), antioxidative genes, and heat shock proteins (HSPs). Our results are consistent with transcriptome detection, indicating that ammonia has a negative effect on immune responses and causes inflammatory injury of the trachea. This study provided baseline information for exploration of the molecular mechanism of NH3-PM2.5 induced respiratory diseases.