Ammonia exposure induced abnormal expression of cytokines and heat shock proteins via glucose metabolism disorders in chicken neutrophils.

Ammonia (NH3) is a highly irritant, alkaline gas. Atmospheric emission of NH3 was recognized as an environmental challenge. As a global issue, the NH3 emission survey with spatially detailed information demonstrated that the sources of atmospheric NH3 include agriculture (livestock wastes, fertilizers) and some industrial activities. As an environmental pollution, excessive NH3 exposure can induce many bird dysfunction. Neutrophils respond to multiple invading pathogens through different mechanisms. In order to investigate the effect of NH3 exposure on broilers' neutrophil, 1-day-old broilers were treated with/without NH3 for 28 days. We extracted neutrophils from peripheral blood of chicken with/without NH3 exposure and subsequently stimulated with PMA. Changes of cytokines and inflammatory bodies, heat shock proteins (HSPs), and glucose metabolism of neutrophil were examined in both cases. We not only explored that the index associated with inflammation changed due to NH3 exposure but also observed the status of neutrophils which was treated with PMA stimulation. After NH3 exposure, IL-1β and IL-6 were significantly increased on broilers neutrophil. Inflammatory-related factors (NLRP3, ASC, and caspase-1) were significantly elevated. The mRNA expression of HSP70 and HSP90 was increased significantly. All glucose metabolism indicators were reduced. In summary, we concluded that NH3 enhanced inflammation and disrupted glucose metabolism, and increased the expression of HSPs and inflammatory factors. In addition, the sensitivity of neutrophils to exogenous stimuli was diminished. This information can not only be used to evaluate the damage of NH3-spiked neutrophils to chickens, but also provide clues for human health pathophysiology caused by excess NH3, providing valuable information for NH3 risk management.