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

Abstract

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.

from Energy Ecology Environment Ambio via Terpsi Hori on Inoreader http://bit.ly/2BC2TRk