Respiratory Diseases Clinic, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.
Unit of Biostatistics, Epidemiology and Public Health, Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padova, Padova, Italy.
Front Immunol. 2021 Oct 18;12:731968. doi: 10.3389/fimmu.2021.731968. eCollection 2021.
Air pollution is a risk factor for respiratory infections and asthma exacerbations. We previously reported impaired Type-I and Type-III interferons (IFN-β/λ) from airway epithelial cells of preschool children with asthma and/or atopy. In this study we analyzed the association between rhinovirus-induced IFN-β/λ epithelial expression and acute exposure to the principal outdoor air pollutants in the same cohort.
We studied 34 children (17asthmatics/17non-asthmatics) undergoing fiberoptic bronchoscopy for clinical indications. Bronchial epithelial cells were harvested by brushing, cultured and experimentally infected with Rhinovirus Type 16 (RV16). RV16-induced IFN-β and λ expression was measured by quantitative real time PCR, as was RV16vRNA. The association between IFNs and the mean exposure to PM10, SO2 and NO in the day preceding bronchoscopy was evaluated using a Generalized Linear Model (GLM) with Gamma distribution.
Acute exposure to PM10 and NO was negatively associated to RV16-induced IFNβ mRNA. For each increase of 1ug/m of NO we found a significative decrease of 2.3x10 IFN-β mRNA copies and for each increase of 1ug/m of PM10 a significative decrease of 1x10 IFN-β mRNA copies. No significant associations were detected between IFN-λ mRNA and NO nor PM10. Increasing levels of NO (but not PM10) were found to be associated to increased RV16 replication.
Short-term exposure to high levels of NO and PM10 is associated to a reduced IFN-β expression by the airway epithelium, which may lead to increased viral replication. These findings suggest a potential mechanism underlying the link between air pollution, viral infections and asthma exacerbations.
空气污染是呼吸道感染和哮喘恶化的危险因素。我们之前报道过，患有哮喘和/或过敏症的学龄前儿童的气道上皮细胞中，I 型和 III 型干扰素（IFN-β/λ）受损。在这项研究中，我们分析了同一队列中鼻病毒诱导的 IFN-β/λ 上皮表达与急性暴露于主要室外空气污染物之间的关联。
我们研究了 34 名（17 名哮喘/17 名非哮喘）因临床指征而行纤维支气管镜检查的儿童。通过刷取收集支气管上皮细胞，进行培养并进行实验性鼻病毒 16 型（RV16）感染。通过定量实时 PCR 测量 RV16 诱导的 IFN-β 和 λ 表达，以及 RV16vRNA。使用广义线性模型（GLM）与伽马分布评估 IFN 与支气管镜检查前一天的 PM10、SO2 和 NO 的平均暴露之间的关联。
急性暴露于 PM10 和 NO 与 RV16 诱导的 IFNβ mRNA 呈负相关。每增加 1μg/m 的 NO，我们发现 IFN-β mRNA 拷贝数显著减少 2.3x10，而每增加 1μg/m 的 PM10，IFN-β mRNA 拷贝数显著减少 1x10。未发现 IFN-λ mRNA 与 NO 或 PM10 之间存在显著相关性。发现 NO（但不是 PM10）水平升高与 RV16 复制增加有关。
短期暴露于高水平的 NO 和 PM10 与气道上皮细胞 IFN-β 表达减少有关，这可能导致病毒复制增加。这些发现提示了空气污染、病毒感染和哮喘恶化之间关联的潜在机制。
