Immune-mediated control of epithelial integrity: Does the immune response to influenza infection cause long-term changes in lung function?

免疫介导的上皮完整性控制：对流感感染的免疫反应是否会导致肺功能的长期变化？

• 批准号: 2290728
• 金额: --
• 依托单位: University of Glasgow
• 依托单位国家: 英国
• 项目类别: Studentship
• 财政年份: 2019
• 资助国家: 英国
• 起止时间: 2019 至 无数据
• 项目状态: 已结题
• 来源: https://gtr.ukri.org/projects?ref=studentship-2290728
• 关键词: Immune; mediated; control; epithelial; integrity

Studentship strategic priority area:Basic Bioscience Underpinning HeathKeywords:Lung, influenza, immunity, cytokines, repairAbstract: Influenza virus infection causes extensive lung damage, caused both by the virus and by the immune response. Surviving influenza requires a careful balance between factors that promote immunity and eradicate the virus, and factors that limit the immune response and minimise collateral damage to the lung. One way to limit damage and reduce disease is to drive an active process of repair and regeneration in the lung, and specifically in the airway epithelium - the cells that line the airways and provide the essential gas exchange as we breathe. In this project we will examine which signalling molecules of the immune system are released into the lung during the immune response to influenza virus infection, and how these signals affect epithelial repair and regeneration durign and after infection. We hypothesise that immune signals are essential to maintain barrier integrity in the lung and to enable gas exchange to continue. Previous evidence suggests that repaired epithelium, after infection, is different to the original epithelium, and we suspect that these changes may contribute to multiple pulmonary disorders including secondary infections, increased sensitisation to allergens, and long-term fibrosis. Our aim is to investigate the role of regulatory immune signals in directing the process of epithelial repair during influenza virus infection, and in the long-term consequences.

学生战略优先领域：基础生物科学支撑健康关键词：肺，流感，免疫，细胞因子，修复摘要：流感病毒感染引起广泛的肺损伤，既由病毒引起，也由免疫反应引起。存活的流感需要在促进免疫和根除病毒的因素与限制免疫反应和将对肺部的附带损害降至最低的因素之间仔细平衡。限制损伤和减少疾病的一种方法是在肺中推动一个活跃的修复和再生过程，特别是在呼吸道上皮细胞--这些细胞排列在呼吸道内，并在我们呼吸时提供必要的气体交换。在这个项目中，我们将研究在对流感病毒感染的免疫反应中，免疫系统的哪些信号分子被释放到肺部，以及这些信号在感染期间和感染后如何影响上皮修复和再生。我们假设免疫信号对维持肺内屏障的完整性和使气体交换继续是必不可少的。以前的证据表明，感染后修复的上皮与原始上皮不同，我们怀疑这些变化可能导致多种肺部疾病，包括继发性感染、对变应原的敏感性增加和长期纤维化。我们的目的是研究调节性免疫信号在流感病毒感染过程中指导上皮修复过程中的作用，以及在长期后果中的作用。