Kilani Muna M, Mohammed Kamal A, Nasreen Najmunnisa, Hardwick Joyce A, Kaplan Mark H, Tepper Robert S, Antony Veena B
Indiana University Medical Center, Indianapolis, USA.
Chest. 2004 Jul;126(1):186-91. doi: 10.1378/chest.126.1.186.
Respiratory syncytial virus (RSV)-induced diseases are mediated through active cytokines released during infection. We hypothesized that RSV infection causes bronchial epithelial monolayer permeability in vitro via induction of vascular endothelial growth factor (VEGF).
Human bronchial epithelial cells were infected with RSV. In some cultures, VEGF antibody was included to block VEGF response; in other cultures, palivizumab was added to block RSV infection. Permeability was assessed in real-time using electric cell-substrate impedance sensing. VEGF release was assessed using enzyme-linked immunosorbent assay. Gap formation was assessed using live cell imaging.
RSV-infected cells demonstrated a decrease in the resistance of the monolayer indicating an increase in permeability; this increase was blocked with VEGF-specific antibody, and palivizumab. Intercellular gap formation developed in RSV-infected epithelial monolayers.
RSV increases permeability of the bronchial airway epithelial monolayer via VEGF induction.
呼吸道合胞病毒（RSV）诱导的疾病是通过感染期间释放的活性细胞因子介导的。我们假设RSV感染通过诱导血管内皮生长因子（VEGF）在体外导致支气管上皮单层通透性增加。
用人支气管上皮细胞感染RSV。在一些培养物中，加入VEGF抗体以阻断VEGF反应；在其他培养物中，加入帕利珠单抗以阻断RSV感染。使用电细胞基质阻抗传感实时评估通透性。使用酶联免疫吸附测定评估VEGF释放。使用活细胞成像评估间隙形成。
RSV感染的细胞显示单层电阻降低，表明通透性增加；这种增加被VEGF特异性抗体和帕利珠单抗阻断。RSV感染的上皮单层中出现细胞间间隙形成。
RSV通过诱导VEGF增加支气管气道上皮单层的通透性。
