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TRIM46通过调节SLC7A11无化,加速H1N1流感病毒诱导的铁和炎症反应

Chao Zhou¹, Genchong Bao², Yanfei Chen³

¹Department of Infection, The People's Hospital of Danyang, Affiliated Danyang Hospital of Nantong University, Danyang, China.

Journal of bioenergetics and biomembranes

|November 12, 2024

概括

三方基因含蛋白46 (TRIM46) 通过降低溶解物载体家族7成员11 (SLC7A11) 的稳定性,加剧了流感A (H1N1) 感染. 针对TRIM46可能为H1N1引起的呼吸道疾病提供一种新的治疗策略.

科学领域:

病毒学病毒学
分子生物学分子生物学
免疫学免疫学免疫学

背景情况:

流感A (H1N1) 导致全球显著的发病率和死亡率.
三方基因含蛋白46 (TRIM46) 具有抗病毒性质.
TRIM46在H1N1病变发生过程中的确切作用尚不清楚.

研究的目的:

研究TRIM46在A型流感 (H1N1) 病毒感染中的作用和机制.
在H1N1感染期间探索TRIM46和溶解物载体家族7成员11 (SLC7A11) 之间的关系.
评估针对H1N1引起的肺损伤中TRIM46的治疗潜力.

主要方法:

实时定量PCR (RT-qPCR) 和西部斑点检测测量TRIM46,SLC7A11以及病毒核蛋白mRNA和蛋白质水平.
细胞计数套件-8 (CCK-8),病毒性 (TCID50),反应性氧物种 (ROS),细胞内铁,马隆迪化物 (MDA) 和谷氨 (GSH) 测试以评估细胞反应.
循环赫西米德 (CHX) 追逐试验以确定SLC7A11的稳定性和共同免疫沉 (CoIP) 试验以验证蛋白质相互作用.
在体内研究使用H1N1挑战小鼠来评估肺损伤.

主要成果:

在H1N1感染期间,TRIM46表达显著上调,而SLC7A11表达下降.
降低TRIM46的调节抑制了H1N1复制,ferroptosis和感染细胞中的炎症.
TRIM46促进了SLC7A11的无所不在,降低了它的稳定性,并导致H1N1的病原性.
在体内,TRIM46敲击减轻了H1N1引起的肺损伤.

结论:

TRIM46在促进流感A (H1N1) 病毒感染方面发挥着至关重要的作用.
TRIM46通过促进SLC7A11的无处不在和不稳定性,为H1N1病变产生作出贡献.
针对TRIM46是一个有希望的治疗策略,可以改善H1N1患者的治疗结果.

关键词:

急性肺损伤是什么?急性肺损伤是什么?铁化是铁化的一种.流感是一种H1N1流感.在 SLC7A1111 中.在 TRIM46 中,我们可以使用 TRIM46.

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