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基素乙化调节ORMDL3表达介导的NLRP3炎症酶在RSV过敏恶化小鼠期间的过度表达

Qi Cheng¹, Fanghan He², Wenqi Zhao¹

¹Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, China.

Journal of cellular physiology

|October 25, 2023

概括

婴儿的呼吸道同胞性病毒 (RSV) 感染可能会导致胞状1样蛋白3 (ORMDL3) 的过度表达,增加反复喘息的风险. 这一过程涉及NLRP3炎症酶激活和基因素乙化,可用于喘治疗.

科学领域:

免疫学免疫学免疫学
呼吸系统医学呼吸系统医学
分子生物学分子生物学

背景情况:

早期的呼吸道同胞性病毒 (RSV) 感染与喘的发展有关.
在RSV诱导的喘中,欧罗索莫科伊德1-样蛋白3 (ORMDL3) 和NOD样受体蛋白3 (NLRP3) 炎症组的作用需要进一步阐明.
希斯乙化可能在这种途径中发挥调节作用.

研究的目的:

为了调查RSV感染,ORMDL3和婴儿的复发性喘息之间的联系.
为了确定ORMDL3过度表达是否会诱导喘中的NLRP3炎症酶激活.
探索素乙化,特别是HAT p300在调节ORMDL3及其下游效应中的作用,并评估p300抑制的治疗潜力.

主要方法:

对RSV诱导的支气管炎的婴儿进行临床数据分析.
使用感染RSV的支气管上皮细胞 (BEAS-2B) 的体外研究.
在体内研究,使用小鼠模型重复RSV感染和卵蛋白敏感化/挑战 (rRSV + OVA).
评估ORMDL3,NLRP3炎症酶和组蛋白乙化标志物.
与ORMDL3-小干扰RNA和HAT p300抑制剂C646.6的干预.

主要成果:

ORMDL3的过度表达被确定为RSV支气管炎后婴儿复发性喘息的独立风险因素.
实验室和体内模型表明,RSV感染导致ORMDL3和NLRP3炎症酶过度表达和基因组过乙化.
ORMDL3直接诱导了NLRP3炎症酶表达.
抑制ORMDL3或HAT p300 (使用C646) 在rRSV+OVA小鼠模型中显著降低了NLRP3炎症酶激活和肺炎炎症.
RSV通过基因素过乙化激活ORMDL3,随后诱导NLRP3炎症酶表达.

结论:

在生命早期的RSV感染促进ORMDL3过度表达通过基因素过化,导致NLRP3炎症酶激活.
ORMDL3 是一个关键的调解者,将RSV感染与复发性喘息和喘病原体联系起来.
抑制HAT p300提供了一种潜在的治疗策略,通过向ORMDL3-NLRP3炎症酶轴来缓解RSV诱导的呼吸道炎症和喘.

关键词:

在NLRP3炎症酶体中,NLRP3炎症这就是ORMDL3的意思.这就是为什么RSV RSV.喘喘是一种生命早期的病毒感染病毒感染在P300上,P300是P300.

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