Asthma is characterised by an aggravated immune response to respiratory viral infections. This phenomenon is a clinically well-recognised driver of acute exacerbations, but how different phenotypes of asthma respond immunologically to viruses is unclear.

To describe the association between different phenotypes and severity of asthma and bronchial epithelial immune responses to viral stimulation.

In the Immunoreact study, healthy subjects (n=10) and 50 patients with asthma were included; 30 (60%) were atopic, and 34 (68%) were eosinophilic; 14 (28%) had severe asthma. All participants underwent bronchoscopy with collection of bronchial brushings. Bronchial epithelial cells (BECs) were expanded and stimulated with the viral replication mimic poly (I:C) (Toll-like receptor (TLR)3 agonist) in vitro. The expression of TLR3-induced pro-inflammatory and antiviral responses of BECs were analysed using reverse transcriptase quantitative PCR and multiplex ELISA and compared across asthma phenotypes and severity of disease.

Patients with atopic asthma had increased induction of interleukin (IL)-4, interferon (IFN)-β, IL-6, tumour necrosis factor-α, and IL-1β after poly (I:C) stimulation compared to non-atopic patients, whereas in patients with eosinophilic asthma only IL-6 and IL-8 induction was higher than in non-eosinophilic asthma. Patients with severe asthma displayed a decreased antiviral IFN-β, and increased expression of IL-8, most pronounced in atopic and eosinophilic asthmatics. Furthermore, induction of IL-33 in response to poly (I:C) was increased in severe atopic and in severe eosinophilic asthma, but thymic stromal lymphopoietin only in severe eosinophilic asthma.

The bronchial epithelial immune response to a viral mimic stimulation differs between asthma phenotypes and severities, which may be important to consider when targeting novel asthma treatments.

哮喘的特征是对呼吸道病毒感染的免疫反应加重。这种现象是临床公认的急性加重驱动因素，但哮喘的不同表型如何对病毒产生免疫反应尚不清楚。

描述不同表型与哮喘严重程度和支气管上皮对病毒刺激的免疫反应之间的关联。

在 Immunoreact 研究中，包括健康受试者（n=10）和 50 名哮喘患者；30 例 (60%) 为特应性，34 例 (68%) 为嗜酸性粒细胞；14 (28%) 人患有严重哮喘。所有参与者都接受了支气管镜检查并收集了支气管刷。体外扩增支气管上皮细胞 (BEC) 并用病毒复制模拟多聚 (I:C)（Toll 样受体 (TLR)3 激动剂）刺激。使用逆转录酶定量 PCR 和多重 ELISA 分析 TLR3 诱导的 BEC 促炎和抗病毒反应的表达，并比较哮喘表型和疾病严重程度。

与非特应性哮喘患者相比，特应性哮喘患者在多 (I:C) 刺激后对白细胞介素 (IL)-4、干扰素 (IFN)-β、IL-6、肿瘤坏死因子-α 和 IL-1β 的诱导增加，而在嗜酸性哮喘患者中，只有 IL-6 和 IL-8 诱导高于非嗜酸性哮喘患者。患有严重哮喘的患者表现出抗病毒 IFN-β 降低，IL-8 表达增加，在特应性和嗜酸性哮喘患者中最为明显。此外，在重度特应性哮喘和重度嗜酸性粒细胞哮喘中，IL-33 响应 poly (I:C) 的诱导增加，但胸腺基质淋巴细胞生成素仅在重度嗜酸性粒细胞哮喘中增加。

支气管上皮对病毒模拟刺激的免疫反应因哮喘表型和严重程度而异，这在针对新型哮喘治疗时可能很重要。