Tight junctions in pulmonary epithelia during lung inflammation

详细信息    查看全文

• 作者：Oliver H. Wittekindt
• 关键词：Lung ; Inflammation ; Asthma ; COPD ; ARDS ; Tight junctions
• 刊名：Pflügers Archiv - European Journal of Physiology
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：469
• 期：1
• 页码：135-147
• 全文大小：2231KB
• 刊物主题：Human Physiology; Molecular Medicine; Neurosciences; Cell Biology; Receptors;
• 出版者：Springer Berlin Heidelberg
• ISSN：1432-2013
• 卷排序：469

文摘

Inflammatory lung diseases like asthma bronchiale, chronic obstructive pulmonary disease and allergic airway inflammation are widespread public diseases that constitute an enormous burden to the health systems. Mainly classified as inflammatory diseases, the treatment focuses on strategies interfering with local inflammatory responses by the immune system. Inflammatory lung diseases predispose patients to severe lung failures like alveolar oedema, respiratory distress syndrome and acute lung injury. These life-threatening syndromes are caused by increased permeability of the alveolar and airway epithelium and exudate formation. However, the mechanism underlying epithelium barrier breakdown in the lung during inflammation is elusive. This review emphasises the role of the tight junction of the airway epithelium as the predominating structure conferring epithelial tightness and preventing exudate formation and the impact of inflammatory perturbations on their function.