南美超级胎牛血清999尝鲜特惠
转染试剂低至5折
基质胶阶梯特惠
积分商城,好礼送不停
南美超级胎牛血清999尝鲜特惠
转染试剂低至5折
基质胶阶梯特惠
积分商城,好礼送不停
分子生物学
IVD分子诊断
细胞培养与分析
蛋白研究
细胞因子
重组蛋白
抗体
高通量测序建库
病原检测UCF系列
生物医药
工具酶
抑制剂激活剂与常用试剂
仪器
耗材

鸡败血支原体通过gga-miR-365-3p/SOCS5/STATs轴逃逸宿主免疫应答机制研究

Mycoplasma gallisepticum escapes the host immune response via gga-miR-365-3p/SOCS5/STATs axis

Wang Yingjie, Han Yun, Wang Lulu, Zou Mengyun, Sun Yingfei, Sun Huanling, Guo Qiao, Peng Xiuli

Journal:VETERINARY RESEARCH

IF:3.83

DOI:10.1186/s13567-022-01117-x

PMID:36471418

Published:2022-12-05

research field:肿瘤学分子生物学非编码RNA研究细胞生物学癌症生物学基因调控

Abstract

A disruption in the expression of gga-miR-365-3p was confirmed in the Mycoplasma gallisepticum (MG)-infected Chicken primary alveolar type II epithelial (CP-II) cells based on previous sequencing results, but the role it plays in the infection was unclear. In the present study, we demonstrate that MG evaded cellular host immunity via a gga-miR-365-3p/SOCS5-JAK/STATs negative feedback loop. Specifically, we found that at the initial stage of MG infection in cells, gga-miR-365-3p was rapidly increased and activated the JAK/STAT signaling pathway by inhibiting SOCS5, which induced the secretion of inflammatory factors and triggered immune response against MG infection. Over time, though, the infection progressed, MG gradually destroyed the immune defences of CP-II cells. In late stages of infection, MG escaped host immunity by reducing intracellular gga-miR-365-3p and inhibiting the JAK/STAT pathway to suppress the secretion of inflammatory factors and promote MG adhesion or invasion. These results revealed the game between MG and host cell interactions, providing a new perspective to gain insight into the pathogenic mechanisms of MG or other pathogens. Meanwhile, they also contributed to novel thoughts on the prevention and control of MG and other pathogenic infections, shedding light on the immune modulating response triggered by pathogen invasion and their molecular targeting.Graphic Abstract

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