Quantitative proteomic analysis of trachea in fatting pig exposed to ammonia.

Ammonia (NH3) is considered as the main pollutant in livestock houses and air environment, and its adverse effects on animal and human health have attracted widespread attention. However, trachea proteomics respond to NH3 is lacking, which is crucial to understanding how NH3 induces respiratory damage. In this study, we performed labeled quantitative proteomic (TMT-MS) analysis in the trachea of fatting pigs exposed to NH3 for 30 days. The proteomic results were then validated by Immunohistochemistry (IHC) and Parallel Reaction Monitoring (PRM). The results showed that a total of 126 differentially abundant proteins (DAPs) were identified (fold change <0.83 or > 1.2 and P < 0.05), including 70 differentially up-regulated proteins (DUPs) and 56 differentially down-regulated proteins (DDPs). These proteins were mainly located in intracellular regions and involved in immune response, metabolism and protein synthesis. The results of DAPs (EHHADH, RPL28, SLC25A6, TUBB6, CD14, CTSS, RPS11, RPL19, SLC25A5, RPS8, FABP3, RPL21, RPL34, RPL32, PDIA3, FBP1, HSPH1, SAR1A and SEC24C) verified by IHC and PRM were consistent with the proteomic results. The results of this study provided a basis and a novel insight for understanding the mechanism of NH3-induced tracheal injury. SIGNIFICANCE: Ammonia (NH3) is considered as the main pollutant in livestock houses and air environment, and its adverse effects on animal and human health have attracted widespread attention. However, trachea proteomics respond to NH3 is lacking, which is crucial to understanding how NH3 induces respiratory damage. Therefore, in this study, labeled quantitative proteomics (TMT-MS) was used to detect trachea tissue samples from finishing pigs in NH3 exposure group and control group, and PRM method was used to further verify the highly abundant proteins in NH3 exposure samples, so as to identify new diagnostic markers for NH3 poisoning. The results of this study provided a basis and a novel insight for understanding the molecular pathological mechanism of NH3-induced tracheal injury.