PT  - JOURNAL ARTICLE
AU  - LD Martin
AU  - LG Rochelle
AU  - BM Fischer
AU  - TM Krunkosky
AU  - KB Adler
TI  - Airway epithelium as an effector of inflammation: molecular regulation of secondary mediators
AID  - 10.1183/09031936.97.10092139
DP  - 1997 Sep 01
TA  - European Respiratory Journal
PG  - 2139--2146
VI  - 10
IP  - 9
4099  - http://erj.ersjournals.com/content/10/9/2139.short
4100  - http://erj.ersjournals.com/content/10/9/2139.full
SO  - Eur Respir J1997 Sep 01; 10
AB  - Deleterious environmental stimuli cause the airway epithelium to respond with increased secretions of mucus, reaction of oxygen/nitrogen species, changes in ciliary beating, and the influx of inflammatory cells. The epithelium is a target for factors released by infiltrating inflammatory cells, and has recently been shown to serve as an effector of such inflammation. Molecular mechanisms regulating production of secondary inflammatory mediators (cytokines, lipid mediators, and reactive oxygen/nitrogen species) have yet to be fully described. This report reviews the production of secondary mediators by epithelial cells and by airway epithelium. Lipid mediators are enzymatically produced by the airway epithelium in response to primary mediators. Molecular mechanisms regulating the production of cyclo-oxygenase, lipoxygenase and prostaglandin synthase are discussed, along with the potential of lipid mediators to produce inflammation. The molecular regulation of nitric oxide production is also described in the context of its role as a signalling molecule in pathways regulating secretion of mucus, ciliary motion, and intercellular adhesion molecule-1 (ICAM-1) expression. The production of cytokines by the airway epithelium is shown to play a role in causing inflammation associated with respiratory diseases. Particular attention is paid to molecular mechanisms governing the expression of tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and interleukin-8 (IL-8).