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IL-13通过抑制ACE2介导的病毒结合和细胞进入来保护上皮细胞免受SARS-CoV-2感染

Vadim Pivniouk^1,2,3, Oksana Pivniouk², Jennifer L Uhrlaub⁴

¹Department of Cellular and Molecular Medicine, The University of Arizona, Tucson, AZ 85721, United States.

|November 24, 2025

概括

2型喘细胞因特鲁金13 (IL-13) 通过抑制呼吸道上皮细胞中的ACE2表达来降低对SARS-CoV-2感染的易感性. 这种机制保护细胞免受病毒进入和感染.

科学领域:

免疫学免疫学免疫学
病毒学病毒学
细胞生物学细胞生物学

背景情况:

严重急性呼吸道综合征冠状病毒2 (SARS-CoV-2) 通过与ACE2结合的尖端蛋白感染呼吸道上皮细胞.
过敏性喘患者表现出有争议的,机理上不清楚的,对COVID-19的敏感性降低.
之前的研究表明,喘性气道中的ACE2mRNA降低,IL-13抑制ACE2表达.

研究的目的:

研究IL-13对上皮细胞中SARS-CoV-2感染步骤的影响.
阐明2型炎症,ACE2表达和SARS-CoV-2感染之间的关系.
确定IL-13是否影响S蛋白与ACE2结合以及ACE2介导的病毒入口.

主要方法:

利用复合IL-13治疗人类上皮细胞.
评估IL-13对SARS-CoV-2 S蛋白与ACE2结合的影响2.
评估IL-13对ACE2介导的病毒输入的影响.
比较IL-13对ACE2-依赖性进入和通过异质促进体进入的影响.

主要成果:

再组合IL-13显著抑制了S蛋白与ACE2的结合和ACE2介导的SARS-CoV-2的进入.
IL-13的抑制作用与抑制的ACE2转录有关.
当ACE2表达由IL-13不响应的促进体驱动时,IL-13不会抑制病毒的进入.

结论:

IL-13保护上皮细胞免受SARS-CoV-2感染.
保护主要通过IL-13诱导的抑制ACE2表达的介导.
这种抑制阻碍病毒进入细胞点,降低感染易感性.

关键词:

在ACE2中,ACE2是ACE2.在 COVID-19 疫情中,这就是SARS-CoV-2病毒.皮质细胞是表皮细胞.这是一种2型炎症.

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