PI3K/AKT/mTOR通路
自噬
穿心莲内酯
蛋白激酶B
生物
体内
炎症体
微生物学
鸡败血症支原体
穿心莲
免疫系统
信号转导
促炎细胞因子
肿瘤坏死因子α
炎症
细胞凋亡
免疫学
细胞生物学
支原体
药理学
医学
生物化学
生物技术
替代医学
病理
作者
Tengfei Wang,Yufei Xiao,Ronglong Luo,Yingjie Wang,Mengyun Zou,Yingfei Sun,Lulu Wang,Qiao Guo,Xiuli Peng
标识
DOI:10.1016/j.intimp.2022.109419
摘要
Mycoplasma gallisepticum (MG) is a pathogenic microorganism that causes chronic respiratory disease (CRD). MG infection has a serious negative impact on the poultry industry. Andrographolide (AG) is known to regulate immune responses, antimicrobial infections, and anti-inflammatory responses. However, the underlying molecular mechanisms of AG action in MG-infected chickens remain unclear. Hence, we constructed models of MG infection by using chickens and chicken macrophage-like (HD11) cells in vivo and in vitro, respectively. The results showed that AG significantly inhibited the mRNA and protein expression of the toxic adhesion protein pMGA1.2 in vivo and in vitro. Meanwhile, AG treatment significantly decreased the mRNA expression of pro-inflammatory such as interleukin-6 (IL-6) and interleukin- 1β (IL-1β), and increased the mRNA expression of an anti-inflammatory such as interleukin-10 (IL-10) and transforming growth factor beta (TGF-β) in vivo and in vitro. Furthermore, AG treatment down-regulated inflammasome NLRP3 and apoptosis genes caspase3 and caspase9, and up-regulated autophagy protein light chain 3 (LC3) by regulating the PI3K/Akt signaling pathway in vitro. Our results suggest that AG can reduce the expression of NLRP3 and alleviate the inflammatory response from MG infection by inducing autophagy, probably by modulating PI3K/Akt signaling pathway. This study demonstrates that AG can be used as a specific target to prevent and treat MG infection effectively.
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