Wang Guangju, Liu Qingxiu, Zhou Ying, Feng Jinghai, Zhang Minhong
State Key Laboratory of Animal Nutrition, Institute of Animal Sciences, Chinese Academy of Agricultural Sciences, Beijing 100193, China.
Animals (Basel). 2022 Jan 21;12(3):261. doi: 10.3390/ani12030261.
Atmospheric ammonia is one of the main environmental stressors affecting the performance of broilers. Previous studies demonstrated that high levels of ammonia altered pulmonary microbiota and induced inflammation. Research into the lung-brain axis has been increasing in recent years. However, the molecular mechanisms in pulmonary microbiota altered by ambient ammonia exposure on broilers and the relationship between microflora, inflammation, and neurotransmitters are still unknown. In this study, a total of 264 Arbor Acres commercial meal broilers (21 days old) were divided into 4 treatment groups (0, 15, 25, and 35 ppm group) with 6 replicates of 11 chickens for 21 days. At 7 and 21 D during the trial period, the lung tissue microflora was evaluated by 16S rDNA sequencing, and the content of cytokines (IL-1β, IL-6, and IL-10) and norepinephrine (NE), 5-hydroxytryptamine (5-HT) in lung tissue were measured. Correlation analysis was established among lung tissue microflora diversity, inflammatory cytokines, and neurotransmitters. Results showed that the broilers were not influenced after exposure to 15 ppm ammonia, while underexposure of 25 and 35 ppm ammonia resulted in significant effects on pulmonary microflora, inflammatory cytokines, and neurotransmitters. After exposure to ammonia for 7 and 21 days, both increased the proportion of Proteobacteria phylum and the contents of IL-1β and decreased the content of 5-HT. After exposure to ammonia for 7 days, the increase in Proteobacteria in lung tissue was accompanied by a decrease in 5-HT and an increase in IL-1β. In conclusion, the microflora disturbance caused by the increase in Proteobacteria in lung tissue may be the main cause of the changes in inflammatory cytokines (IL-1β) and neurotransmitters (5-HT), and the damage caused by ammonia to broiler lungs may be mediated by the lung-brain axis.
大气氨是影响肉鸡生产性能的主要环境应激源之一。先前的研究表明，高浓度氨会改变肺部微生物群并引发炎症。近年来，对肺-脑轴的研究不断增加。然而，环境氨暴露改变肉鸡肺部微生物群的分子机制以及微生物群、炎症和神经递质之间的关系仍不清楚。在本研究中，将总共264只21日龄的爱拔益加商品肉仔鸡分为4个处理组（0、15、25和35 ppm组），每组11只鸡，重复6次，为期21天。在试验期的第7天和第21天，通过16S rDNA测序评估肺组织微生物群，并测定肺组织中细胞因子（IL-1β、IL-6和IL-10）以及去甲肾上腺素（NE）、5-羟色胺（5-HT）的含量。对肺组织微生物群多样性、炎性细胞因子和神经递质进行相关性分析。结果表明，暴露于15 ppm氨后肉鸡未受影响，而25和35 ppm氨暴露不足对肺部微生物群、炎性细胞因子和神经递质产生了显著影响。暴露于氨7天和21天后，变形菌门的比例均增加，IL-1β的含量增加，5-HT的含量降低。暴露于氨7天后，肺组织中变形菌的增加伴随着5-HT的减少和IL-1β的增加。总之，肺组织中变形菌增加导致的微生物群紊乱可能是炎性细胞因子（IL-1β）和神经递质（5-HT）变化的主要原因，氨对肉鸡肺部造成的损伤可能是由肺-脑轴介导的。
