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禽舍中的细颗粒物2.5与[未提及的物质]协同作用,通过核因子κB途径加重小鼠肺部炎症。

PM2.5 in poultry houses synergizes with to aggravate lung inflammation in mice through the NF-κB pathway.

作者信息

Li Meng, Wei Xiuli, Li Youzhi, Feng Tao, Jiang Linlin, Zhu Hongwei, Yu Xin, Tang Jinxiu, Chen Guozhong, Zhang Jianlong, Zhang Xingxiao

机构信息

College of Life Science, Ludong University, Yantai 264000, China.

Shandong Provincial Key Laboratory of Quality Safty Monitoring and Risk Assessment for Animal Products, Ji'nan 250022, China.

出版信息

J Vet Sci. 2020 May;21(3):e46. doi: 10.4142/jvs.2020.21.e46.

Abstract

BACKGROUND

High concentrations of particulate matter less than 2.5 μm in diameter (PM2.5) in poultry houses is an important cause of respiratory disease in animals and humans. is an opportunistic pathogen that can induce severe respiratory disease in animals under stress or with abnormal immune functions. When excessively high concentrations of PM2.5 in poultry houses damage the respiratory system and impair host immunity, secondary infections with can occur and produce a more intense inflammatory response, resulting in more severe lung injury.

OBJECTIVES

In this study, we focused on the synergistic induction of inflammatory injury in the respiratory system and the related molecular mechanisms induced by PM2.5 and in poultry houses.

METHODS

High-throughput 16S rDNA sequence analysis was used for characterizing the bacterial diversity and relative abundance of the PM2.5 samples, and the effects of PM2.5 and stimulation on inflammation were detected by and .

RESULTS

Sequencing results indicated that the PM2.5 in poultry houses contained a high abundance of potentially pathogenic genera, such as (2.94%). The lung tissues of mice had more significant pathological damage when co-stimulated by PM2.5 and , and it can increase the expression levels of interleukin (IL)-6, IL-8, and tumor necrosis factor-α through nuclear factor (NF)-κB pathway and .

CONCLUSIONS

The results confirmed that poultry house PM2.5 in combination with could aggravate the inflammatory response and cause more severe respiratory system injuries through a process closely related to the activation of the NF-κB pathway.

摘要

背景

禽舍中直径小于2.5微米的颗粒物(PM2.5)浓度过高是动物和人类呼吸道疾病的重要原因。[病原体名称]是一种机会致病菌,可在应激或免疫功能异常的动物中诱发严重呼吸道疾病。当禽舍中PM2.5浓度过高损害呼吸系统并削弱宿主免疫力时,[病原体名称]的继发感染可能发生并产生更强烈的炎症反应,导致更严重的肺损伤。

目的

在本研究中,我们重点关注禽舍中PM2.5和[病原体名称]对呼吸系统炎症损伤的协同诱导作用及其相关分子机制。

方法

采用高通量16S rDNA序列分析对PM2.5样本的细菌多样性和相对丰度进行表征,并通过[检测方法1]和[检测方法2]检测PM2.5和[病原体名称]刺激对炎症的影响。

结果

测序结果表明,禽舍中的PM2.5含有高丰度的潜在致病属,如[属名称](2.94%)。当受到PM2.5和[病原体名称]共同刺激时,小鼠肺组织有更明显的病理损伤,并且它可通过核因子(NF)-κB途径[途径1]和[途径2]增加白细胞介素(IL)-6、IL-8和肿瘤坏死因子-α的表达水平。

结论

结果证实,禽舍PM2.5与[病原体名称]联合可加重炎症反应,并通过与NF-κB途径激活密切相关的过程导致更严重的呼吸系统损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6ac3/7263920/84ccd0c9db13/jvs-21-e46-g001.jpg

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