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Type 2 inflammation modulates ACE2 and TMPRSS2 in airway epithelial cells.
Journal of Allergy and Clinical Immunology ( IF 11.4 ) Pub Date : 2020-05-15 , DOI: 10.1016/j.jaci.2020.05.004
Hiroki Kimura 1 , Dave Francisco 1 , Michelle Conway 1 , Fernando D Martinez 2 , Donata Vercelli 2 , Francesca Polverino 1 , Dean Billheimer 3 , Monica Kraft 1
Affiliation  

Background

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has dramatically changed our world, country, communities, and families. There is controversy regarding risk factors for severe COVID-19 disease. It has been suggested that asthma and allergy are not highly represented as comorbid conditions associated with COVID-19.

Objective

Our aim was to extend our work in IL-13 biology to determine whether airway epithelial cell expression of 2 key mediators critical for SARS-CoV-2 infection, namely, angiotensin-converting enzyme 2 (ACE2) and transmembrane protease, serine 2 (TMPRSS2), are modulated by IL-13.

Methods

We determined effects of IL-13 treatment on ACE2 and TMPRSS2 expression ex vivo in primary airway epithelial cells from participants with and without type 2 asthma obtained by bronchoscopy. We also examined expression of ACE2 and TMPRSS2 in 2 data sets containing gene expression data from nasal and airway epithelial cells from children and adults with asthma and allergic rhinitis.

Results

IL-13 significantly reduced ACE2 and increased TMPRSS2 expression ex vivo in airway epithelial cells. In 2 independent data sets, ACE2 expression was significantly reduced and TMPRSS2 expression was significantly increased in the nasal and airway epithelial cells in type 2 asthma and allergic rhinitis. ACE2 expression was significantly negatively associated with type 2 cytokines, whereas TMPRSS2 expression was significantly positively associated with type 2 cytokines.

Conclusion

IL-13 modulates ACE2 and TMPRSS2 expression in airway epithelial cells in asthma and atopy. This deserves further study with regard to any effects that asthma and atopy may render in the setting of COVID-19 infection.



中文翻译:

2 型炎症调节气道上皮细胞中的 ACE2 和 TMPRSS2。

背景

严重急性呼吸系统综合症冠状病毒 2 (SARS-CoV-2) 极大地改变了我们的世界、国家、社区和家庭。关于严重 COVID-19 疾病的危险因素存在争议。有人提出,哮喘和过敏症并未高度代表与 COVID-19 相关的合并症。

客观的

我们的目标是扩展我们在 IL-13 生物学方面的工作,以确定 2 个关键介质的气道上皮细胞表达是否对 SARS-CoV-2 感染至关重要,即血管紧张素转换酶 2 ( ACE2 ) 和跨膜蛋白酶丝氨酸 2 ( TMPRSS2 ) ), 由 IL-13 调制。

方法

我们确定了 IL-13 治疗对通过支气管镜检查获得的患有和不患有 2 型哮喘的参与者的原发性气道上皮细胞中ACE2TMPRSS2表达的影响。我们还在 2 个数据集中检测了ACE2TMPRSS2的表达,这些数据包含来自患有哮喘和过敏性鼻炎的儿童和成人的鼻腔和气道上皮细胞的基因表达数据。

结果

IL-13 显着降低气道上皮细胞中的ACE2并增加TMPRSS2离体表达。在 2 个独立的数据集中,2 型哮喘和过敏性鼻炎患者的鼻腔和气道上皮细胞中ACE2表达显着降低,TMPRSS2表达显着升高。ACE2表达与 2 型细胞因子显着负相关,而TMPRSS2表达与 2 型细胞因子显着正相关。

结论

IL-13 调节哮喘和特应性气道上皮细胞中ACE2TMPRSS2的表达。关于哮喘和特应性在 COVID-19 感染的情况下可能产生的任何影响,这值得进一步研究。

更新日期:2020-07-03
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