The effect of endotoxin and prostaglandin E2 on the proliferation of keratinocytes in vitro.
Since the rate of epidermal basal cell proliferation appears to be a crucial factor in the development of acquired cholesteatoma, we studied the effect of prostaglandin E2 (PGE2) and endotoxin on the growth of keratinocytes. PGE2 and endotoxins are inflammatory mediators in chronic otitis media. Various concentrations of endotoxin and PGE2 were added to keratinocytes derived from newborn rats. The synthesis of DNA was then studied by incorporation of 3H-thymidine into the keratinocytes. We found that either endotoxin or PGE2 alone inhibited DNA synthesis by keratinocytes, while endotoxin (10 micrograms/ml) and PGE2 (10 ng/ml) together stimulated DNA synthesis by keratinocytes. These findings suggest that inflammatory mediators, such as endotoxin plus PGE2, in chronic otitis media stimulate the growth of epidermal basal cells of cholesteatoma.
D000818:Animals; D001862:Bone Resorption / Q000187:drug effects; D002454:Cell Differentiation / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D002781:Cholesteatoma / Q000473:pathology; D015232:Dinoprostone; D004357:Drug Synergism; D004731:Endotoxins / Q000494:pharmacology*; D000078404:Epidermal Cells; D007633:Keratins; D011458:Prostaglandins E / Q000494:pharmacology*; D051381:Rats; D011917:Rats, Inbred Lew
D004731:Endotoxins; D011458:Prostaglandins E; D007633:Keratins; D015232:Dinoprostone