PubMed Journals: Eur Respir J

  Source:		PMID: 9311517
  Download:	https://erj.ersjournals.com/content/erj/10/9/2139.full.pdf

    		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.

			Author Information
			(1) Dept of Anatomy, Physiological Sciences
			and Radiology, North Carolina State University,
			College of Veterinary Medicine, Raleigh
			27606, USA.

			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]

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