Crespo-Lessmann Astrid, Mateus Eder, Vidal Silvia, Ramos-Barbón David, Torrejón Montserrat, Giner Jordi, Soto Lorena, Juárez Cándido, Plaza Vicente
Respiratory Department, Hospital de la Santa Creu i Sant Pau & Biomedical Research Institute Sant Pau (IIB Sant Pau), Sant Antoni Maria Claret 167, 08025, Barcelona, Spain.
Department of Medicine, Universitat Autònoma de Barcelona, Barcelona, Spain.
Respir Res. 2016 Apr 16;17:41. doi: 10.1186/s12931-016-0355-2.
Emerging data suggest that innate immunity may play a role in asthma, particularly the toll-like receptors (TLRs). Some studies pointed to an involvement of TLRs 2 and 4 in the pathogenesis of allergic asthma, and other studies related TLRs to IgE. However, there are not any studies that have comprehensively evaluated the expression of TLRs 2 and 4 in inflammatory cells, in peripheral blood and induced sputum specimens from asthmatic patients, according to their total serum IgE.
We studied 44 asthmatic patients (15 with high total serum IgE and 29 with normal total serum IgE). On a single visit, all patients underwent: induced sputum, pulmonary function tests, determination of exhaled nitric oxide fraction, venipuncture for blood analysis and skin prick allergy tests. The induced sputum cellularity was analyzed by flow cytometry, where expression of TLRs 2 and 4 was studied using fluorochrome-conjugated monoclonal antibodies.
Asthmatic patients with high total serum IgE showed, a higher percentage of macrophages expressing TLR4 (42.99 % ± 22.49) versus asthmatic patients with normal total serum IgE (28.84 % ± 15.16) (P = 0.048). Furthermore, we observed a correlation (but weak) between the percentage of macrophages expressing TLR4 in induced sputum and the total serum IgE level (R = 0.314; P = 0.040).
Asthmatic subjects with high total serum IgE show increased macrophage expression of TLR4 in induced sputum. This outcome may result from a link between innate immunity and IgE-mediated, adaptive immune responses in asthma, and point to TLR4 as a potential therapeutic target.
新出现的数据表明，固有免疫可能在哮喘中发挥作用，尤其是 Toll 样受体（TLR）。一些研究指出 TLR2 和 TLR4 参与过敏性哮喘的发病机制，其他研究则将 TLR 与 IgE 联系起来。然而，尚无研究根据哮喘患者血清总 IgE 水平，全面评估外周血和诱导痰标本中炎症细胞内 TLR2 和 TLR4 的表达情况。
我们研究了 44 例哮喘患者（15 例血清总 IgE 水平高，29 例血清总 IgE 水平正常）。在一次就诊时，所有患者均接受：诱导痰检查、肺功能测试、呼出一氧化氮分数测定、静脉穿刺采血分析以及皮肤点刺过敏试验。通过流式细胞术分析诱导痰细胞组成，使用荧光素偶联单克隆抗体研究 TLR2 和 TLR4 的表达。
血清总 IgE 水平高的哮喘患者中，表达 TLR4 的巨噬细胞百分比（42.99%±22.49）高于血清总 IgE 水平正常的哮喘患者（28.84%±15.16）（P = 0.048）。此外，我们观察到诱导痰中表达 TLR4 的巨噬细胞百分比与血清总 IgE 水平之间存在相关性（但较弱）（R = 0.314；P = 0.040）。
血清总 IgE 水平高的哮喘患者在诱导痰中巨噬细胞 TLR4 表达增加。这一结果可能源于哮喘中固有免疫与 IgE 介导的适应性免疫反应之间的联系，并提示 TLR4 作为潜在的治疗靶点。
