Halwani Rabih, Al-Kufaidy Roua, Vazquez-Tello Alejandro, Pureza Mary Angeline, BaHammam Ahmed S, Al-Jahdali Hamdan, Alnassar Sami A, Hamid Qutayba, Al-Muhsen Saleh
Prince Naif Center for Immunology Research, department of pediatrics, College of Medicine, King Saud University, Riyadh, Saudi Arabia.
Prince Naif Center for Immunology Research, department of pediatrics, College of Medicine, King Saud University, Riyadh, Saudi Arabia; Pulmonary Medicine Department, University Sleep Disorders Center, College of Medicine, King Saud University, Riyadh, Kingdom of Saudi Arabia.
PLoS One. 2014 Dec 10;9(12):e114604. doi: 10.1371/journal.pone.0114604. eCollection 2014.
IL-17 is a pro-inflammatory mediator that is believed to play a critical role in regulating tissue inflammation during asthma, COPD, as well as other inflammatory disorders. The level of expression of IL-17 has been shown to be upregulated in lung bronchial tissue of asthmatic patients. Several reports have provided further evidence that this cytokine could play a key role in enhancing the migration of inflammatory as well as structural cells of the bronchial lung tissue during asthma and COPD. B cell infiltration to sites of inflammation during inflammatory disorders such as bowel disease, asthma and COPD has been reported. Accordingly, in this study we hypothesized that IL-17 may exert a chemotactic effect on primary B cells during asthma. We observed that B cells from asthmatic patients expressed significantly higher levels of IL-17RA and IL-17RC, compared to those of healthy subjects. Using an in-vitro migration assay, B cells were shown to migrate towards both IL-17A and IL-17F. Interestingly, blocking IL-17A and IL-17F signaling using either anti-IL-17R antibodies or MAP kinase inhibitors prevented in vitro migration of B cell towards IL-17. These observations indicate a direct chemotactic effect of IL-17 cytokines on primary peripheral blood B cells with higher effect being on asthmatic B cells. These findings revealed a key role for IL-17 in enhancing the migration of B cells to the lung tissue during asthma or COPD.
白细胞介素-17（IL-17）是一种促炎介质，据信在哮喘、慢性阻塞性肺疾病（COPD）以及其他炎症性疾病的组织炎症调节中起关键作用。研究表明，哮喘患者肺支气管组织中IL-17的表达水平上调。多项报告进一步证明，这种细胞因子在哮喘和COPD期间增强支气管肺组织炎症细胞和结构细胞的迁移中可能起关键作用。据报道，在诸如肠道疾病、哮喘和COPD等炎症性疾病中，B细胞会浸润到炎症部位。因此，在本研究中，我们假设IL-17在哮喘期间可能对原代B细胞发挥趋化作用。我们观察到，与健康受试者相比，哮喘患者的B细胞表达显著更高水平的IL-17RA和IL-17RC。使用体外迁移试验，结果显示B细胞会向IL-17A和IL-17F迁移。有趣的是，使用抗IL-17R抗体或丝裂原活化蛋白激酶（MAP）抑制剂阻断IL-17A和IL-17F信号可阻止B细胞在体外向IL-17迁移。这些观察结果表明IL-17细胞因子对原代外周血B细胞具有直接趋化作用，对哮喘B细胞的作用更强。这些发现揭示了IL-17在哮喘或COPD期间增强B细胞向肺组织迁移中的关键作用。
