PubMed Journals: Eur Respir J
Source: PMID: 9311517
⇦ ⇨ Eur Respir J. 1997 Sep;10(9):2139-46.
Airway epithelium as an effector of inflammation:
molecular regulation of secondary mediators.
Martin LD(1), Rochelle LG, Fischer BM, Krunkosky
TM, Adler KB.
(1) Dept of Anatomy, Physiological Sciences
and Radiology, North Carolina State University,
College of Veterinary Medicine, Raleigh
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
PMID: 9311517 [Indexed for MEDLINE]