Ammonia induce lung tissue injury in broilers by activating NLRP3 inflammasome via Escherichia/Shigella

被引:70
作者
Liu, Qing Xiu [1 ]
Zhou, Ying [1 ]
Li, Xiu Mei [1 ]
Dan, Dan [1 ]
Xing, Shuang [1 ]
Feng, Jing Hai [1 ]
Zhang, Min Hong [1 ]
机构
[1] Chinese Acad Agr Sci, Inst Anim Sci, State Key Lab Anim Nutr, Beijing 100193, Peoples R China
关键词
ammonia; respiratory tract flora; NLRP3; inflammasome; IL-10; inflammation; INFLUENZA-VIRUS; PUBLIC-HEALTH; COLI; MECHANISMS; CRYSTALS; IMMUNITY; DISEASE; DUST; HAZE;
D O I
10.1016/j.psj.2020.03.019
中图分类号
S8 [畜牧、 动物医学、狩猎、蚕、蜂];
学科分类号
0905 ;
摘要
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-1 beta 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-1 beta 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-1 beta release. These findings provided a reference for the prevention and control of respiratory tract diseases in humans and animals caused by ammonia pollution.
引用
收藏
页码:3402 / 3410
页数:9
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