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) c ells were used to study the response of differentiated airway epitheli al 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 phospholip ase A2 (cPLA2) and prostaglandin H synthase 2 (PGHS2) were upregulated ; as a result prostaglandin E (PGE2) secretion was increased. Subseque nt to the increase in PGE2 mucus secretion increased, suggesting that PGE2 may act as an autocrine regulator of mucus secretion.