Airway epithelial regulation of pulmonary immune homeostasis and inflammation

被引:191
作者
Hallstrand, Teal S. [1 ]
Hackett, Tillie L. [2 ]
Altemeier, William A. [1 ]
Matute-Bello, Gustavo [1 ]
Hansbro, Philip M. [3 ]
Knight, Darryl A. [3 ]
机构
[1] Univ Washington, Div Pulm & Crit Care Med, Dept Med, Seattle, WA 98195 USA
[2] Univ British Columbia, Dept Anesthesiol Pharmacol & Therapeut, Vancouver, BC V5Z 1M9, Canada
[3] Univ Newcastle, Sch Biomed Sci & Pharm, Callaghan, NSW 2308, Australia
关键词
Asthma; Epithelium; Chemokine; Chronic-obstructive; pulmonary disease; Host defense; Tight junctions; THYMIC STROMAL LYMPHOPOIETIN; HOUSE-DUST MITE; TOLL-LIKE RECEPTOR-3; RESPIRATORY SYNCYTIAL VIRUS; COLONY-STIMULATING FACTOR; ACTIVATED PROTEIN-KINASE; MESSENGER-RNA EXPRESSION; DOUBLE-STRANDED-RNA; N-TERMINAL KINASE; STEM-CELL FACTOR;
D O I
10.1016/j.clim.2013.12.003
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Recent genetic, structural and functional studies have identified the airway and lung epithelium as a key orchestrator of the immune response. Further, there is now strong evidence that epithelium dysfunction is involved in the development of inflammatory disorders of the lung. Here we review the characteristic immune responses that are orchestrated by the epithelium in response to diverse triggers such as pollutants, cigarette smoke, bacterial peptides, and viruses. We focus in part on the role of epithelium-derived interleukin (IL)-25, IL-33 and thymic stromal lymphopoietin (TSLP), as well as CC family chemokines as critical regulators of the immune response. We cite examples of the function of the epithelium in host defense and the role of epithelium dysfunction in the development of inflammatory diseases. (c) 2014 Elsevier Inc. All rights reserved.
引用
收藏
页码:1 / 15
页数:15
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