Eicosanoids and Inflammatory cells in Asthma

O’Byrne, Paul M.

doi:10.1007/978-3-0348-7379-6_11

Cited by 1 publication

(1 citation statement)

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“…By contrast, some prostanoids appear to be anti-inflammatory. For example, PGE 2 and prostaglandin I 2 (PGI 2 ) can counteract the bronchoconstrictor effects of other eicosanoids, and may be major components of epithelial-derived relaxing factor [20,21].…”

Section: Lipid Mediatorsmentioning

confidence: 99%

Airway epithelium as an effector of inflammation: molecular regulation of secondary mediators

Martin

Rochelle²,

Fischer³

et al. 1997

Eur Respir J

139

101

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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-α (TNF-α), interleukin-6 (IL-6), and interleukin-8 (IL-8).

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Section: Lipid Mediatorsmentioning

confidence: 99%