Ammonia exposure causes lung injuries and disturbs pulmonary circadian clock gene network in a pig study.

ABSTRACT

Ammonia toxicity to respiratory system in pig faming is of particular concern, but the molecular mechanism remains still unclear. The present study was devoted to assess the impacts of the ammonia exposure on the lung tissues based on a pig study using 80 ppm ammonia exposing to piglets for different days. The histology analysis revealed ammonia exposure induced lung injury and inflammatory response, as indicated by epithelial-mesenchymal transition (EMT), significant thickening of alveolar septa, infiltration of inflammatory cells and excessive mucus production. The transcriptome analysis revealed many more up-regulated genes in exposure groups when compared with the control group, and these genes were significantly enriched in the GO term of extracellular exosome, proteolysis, and regulation of circadian rhythm. The study discovered the induction of seven genes (CRY2, CIART, CREM, NR1D1, NR1D2, PER1 and PER3) that encode repressors of circadian clock. One gene (ARNTL) that encodes activator of circadian clock was down-regulated after ammonia exposure. The results of this study suggest that ammonia exposure disturbed the pulmonary circadian clock gene expression, which may establish new evidence for further understanding the toxicity of ammonia to lungs.