PROSTAGLANDIN E-2 AND INTERLEUKIN-1 CONCENTRATIONS IN NICOTINE-EXPOSED ORAL KERATINOCYTE CULTURES

Oral keratinocytes are the first cells in contact with tobacco compone nts and are capable of producing various inflammatory mediators, inclu ding PGE(2) and IL-1. The purpose of this study was to examine PGE(2) and IL-1 concentrations in nicotine-exposed oral keratinocyte cultures . Gingival keratinocyte cultures were established from healthy gingiva l tissues obtained from 7 subjects. Cultures were divided into 4 group s exposed to serum free medium (control), 0.1 mu M, 10 mu M or 1 mM ni cotine for 4, 24 or 48 h. Using enzyme-linked immunosorbent assays, PG E(2) and IL-1 alpha were quantified in culture supernatants; IL-1 alph a and beta were also measured in lysed cells. A repeated measures anal ysis of variance was used to identify significant differences over tim e and treatment. Nicotine exposure did not significantly alter PGE(2) levels at any given time period; however, PGE(2) quantities declined s ignificantly (p= 0.0001) over time. At both 24 and 48 h, IL-1 alpha co ncentrations in lysates from 1 mM nicotine-exposed cells were signific antly (p < 0.01) greater than those for all other treatments. Interleu kin-1 alpha quantities also declined significantly (p= 0.037) over tim e in the cultures. Interleukin-1 beta concentrations were elevated, al beit not significantly, in the 1 mM treated cells at 24 and 48 h. Cell viability, mass and counts were not affected by nicotine treatment; t hese parameters increased significantly (p < 0.005) over time. In summ ary, nicotine treatment significantly increased IL-1 alpha concentrati ons in cultured keratinocytes; however, PGE(2) synthesis was not alter ed. Elevated IL-1 production by keratinocytes may have implications in tobacco-induced lesions, given the central role IL-1 plays in tissue response to injury.