Abstract
The airway epithelial cell barrier serves as the main site of replication for most of the common respiratory viruses and is thereby the first line of defense against these viruses. Host epithelial cells are specially enriched for pattern recognition receptors that activate immune response genes to limit viral replication. A prominently expressed set of these genes encodes cytokines that orchestrate key aspects of host defense, such as recruitment of immune cells and repair of epithelial cell damage. Under some circumstances, airway epithelial cells may be programmed to release cytokines (notably IL-33) that activate a type 2 immune response, which in excess might contribute to the development of chronic obstructive lung disease. Moreover, long-term epithelial progenitor cells with this capability may explain an ongoing susceptibility to lung disease in response to acute respiratory infection or other types of inhaled danger signals. The mucosal airway epithelial cell can thereby mediate a beneficial response for host defense and a detrimental response leading to inflammatory disease.
Original language | English |
---|---|
Title of host publication | Mucosal Immunology |
Subtitle of host publication | Fourth Edition |
Publisher | Elsevier Inc. |
Pages | 1013-1021 |
Number of pages | 9 |
Volume | 1-2 |
ISBN (Electronic) | 9780124159754 |
ISBN (Print) | 9780124158474 |
DOIs | |
State | Published - Apr 1 2015 |
Keywords
- Asthma
- COPD
- Chronic obstructive lung disease
- Epithelial biology
- Host-pathogen interactions
- Innate immunity
- Respiratory disease
- Virology