Tumor necrosis factor alpha stimulates arachidonic acid metabolisms and mucus production in rat tracheal epithelial cell cultures.
Air-liquid interface (ALI) cultures of rat tracheal epithelial (RTE) cells were used to study the response of differentiated airway epithelial cells to the inflammatory cytokine, tumor necrosis factor alpha (TNF alpha). We found that the cultures expressed low levels of TNF alpha receptors. TNF alpha stimulated the AA-cascade: cytoplasmic phospholipase A2 (cPLA2) and prostaglandin H synthase 2 (PGHS2) were upregulated; as a result prostaglandin E (PGE2) secretion was increased. Subsequent to the increase in PGE2 mucus secretion increased, suggesting that PGE2 may act as an autocrine regulator of mucus secretion.
Nettesheim
P
P
National Institute of Environmental Health Sciences, Research Triangle Park, NC 27709, USA.
Bader
T
T
D000818:Animals; D016718:Arachidonic Acid / Q000378:metabolism*; D002478:Cells, Cultured; D015232:Dinoprostone / Q000096:biosynthesis; D004847:Epithelial Cells; D004848:Epithelium / Q000187:drug effects / Q000378:metabolism; D009093:Mucus / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D018124:Receptors, Tumor Necrosis Factor / Q000502:physiology; D014132:Trachea / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology / Q000502:physiology*
D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha; D016718:Arachidonic Acid; D015232:Dinoprostone