Respiratory tract diseases are closely related to atmosphere pollution. Ammonia is one of the harmful pollutants in the atmosphere environment, which has a great threat to human and animal respiratory tract health, but the mechanism of causing diseases is not clear. In this study, broiler lung tissue was used as a model to study the effect of high ammonia on respiratory tract diseases through the relationship between respiratory microflora, NLRP3 inflammasome, and inflammatory factors. For this, we validated the occurrence of lung tissue inflammation under ammonia exposure and detected the lung tissue microbial constituent by 16S rDNA sequencing. Moreover, the relative expression levels of NLRP3 and caspase-1 mRNA and the content of IL-1β and IL-6 were measured. After 7-D ammonia exposure, the proportion of the phylum Proteobacteria and the genus Escherichia/Shigella in lung tissue was significantly increased, the expression levels of NLRP3 and caspase-1 mRNA were significantly increased, and the content of IL-1β in lung tissue and serum was higher than that in the control group. In conclusion, high ammonia induced lung tissue inflammation via increasing the proportion of Escherichia/Shigella , activating NLRP3 inflammasome, and promoting IL-1β release. These findings provided a reference for the prevention and control of respiratory tract diseases in humans and animals caused by ammonia pollution.
This study investigated the effects of ammonia (NH 3 ) exposure (0, 15, 25, and 35 ppm) on growth performance and cytokines in the serum, trachea, and ileum of broilers. A total of 288 22-day-old male broiler chickens were assigned to 4 treatment groups with 6 replicates of 12 chickens for a 21-D trial period. Growth performance and cytokines (IL-1β, IL-6, and IL-10) concentrations in the serum, trachea, and ileum were measured in response to 3, 7, 14, or 21 D of exposure to NH 3 . Correlations between cytokines in the serum, trachea, and ileum and growth performance, and between tracheal and ileal cytokines, were also analyzed. Results showed that exposure to 15 ppm NH 3 did not influence the growth performance, but exposure to both 25 ppm and 35 ppm NH 3 decreased the growth performance compared to that of the control group. Exposure to 15 ppm NH 3 for 3 D increased IL-6 concentrations and induced an inflammatory response in the trachea and ileum, whereas exposure to 15 ppm NH 3 for 7 D increased IL-10 concentrations and induced an anti-inflammatory response in the ileum. Exposure to 25 ppm NH 3 induced an inflammatory response in the serum, trachea, and ileum after 3 D and induced an anti-inflammatory response in the ileum after 7 D. Exposure to 35 ppm NH 3 for 3 D induced both inflammatory and anti-inflammatory responses in the trachea and ileum. Furthermore, increases in cytokines in the serum, trachea, or ileum were accompanied by a decrease in BW, ADFI, ADG, and an increase of feed/gain (F/G) from 7 D to 21 D. In addition, tracheal cytokine, especially IL-1 β , was positively correlated with ileal cytokine IL-1 β . These results indicated that the low growth performance associated with NH 3 exposure may be due in part to an increase in cytokines, and the inflammatory response in the trachea and ileum may be related to cross-talk by cytokines such as IL-6, IL-10, and, in particular, IL-1 β .
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