Rm. Kafoury et al., Induction of inflammatory mediators in human airway epithelial cells by lipid ozonation products, AM J R CRIT, 160(6), 1999, pp. 1934-1942
We have proposed that exposure of epithelial cell membrane lipids in the lu
ng (mainly phospholipids) to ozone will generate lipid ozonation products (
LOP), which could be responsible for the proinflammatory effects of ozone.
The ozonation of phosphocholine, the principal membrane phospholipid, produ
ces a limited number of LOP, including hydroxyhydroperoxides and aldehydes.
We now report that exposure of cultured human bronchial epithelial cells t
o the ozonized 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) prod
uct, 1-palmitoyl-2-(9-oxononanoyl)-sn-glycero-3-phosphocholine (PC-ALD), a
phospholipase A(2) (PLA(2))-stimulatory LOP, resulted in a 113 +/- 11% incr
ease in the amounts of tritiated platelet-activating factor (H-3-PAF) relea
sed apically. H-3-PAF release was also induced by 1-hydroxy-1-hydroperoxyno
nane of ozonized POPC (HHP-C9), a phospholipase C (PLC)stimulatory LOP (134
+/- 40% increase in H-3-PAF). PC-ALD at 10 mu M, but not HHP-C9, induced a
127 +/- 24% increase in prostaglandin E-2 (PGE(2)) release (n = 6, p < 0.0
5). In contrast, HHP-C9, but not PC-ALD, induced interleukin (IL)-6 release
(178 +/- 23% increase, n = 6, p < 0.05) and IL-8 release (101 +/- 23% incr
ease, n = 8,p < 0.05). These results suggest that LOP-dependent release of
proinflammatory mediators may play an important role in the early inflammat
ory response seen during exposure to ozone.