Prostaglandin E-2 and interleukin-1 concentrations in nicotine-exposed oral keratinocyte cultures

Oral keratinocytes are the first cells in contact with tobacco components and are capable of producing various inflammatory mediators, including 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 gingival tissues obtained from 7 subjects. Cultures were divided into 4 groups exposed to serum free medium (control), 0.1 mu M, 10 mu M or 1 mM nicotine for 4, 24 or 48 h. Using enzyme-linked immunosorbent assays, PGE(2) and IL-1 alpha were quantified in culture supernatants; IL-1 alpha and beta were also measured in lysed cells. A repeated measures analysis of variance was used to identify significant differences over time and treatment. Nicotine exposure did not significantly alter PGE(2) levels at any given time period; however, PGE(2) quantities declined significantly (p= 0.0001) over time. At both 24 and 48 h, IL-1 alpha concentrations in lysates from 1 mM nicotine-exposed cells were significantly (p < 0.01) greater than those for all other treatments. Interleukin-1 alpha quantities also declined significantly (p= 0.037) over time in the cultures. Interleukin-1 beta concentrations were elevated, albeit not significantly, in the 1 mM treated cells at 24 and 48 h. Cell viability, mass and counts were not affected by nicotine treatment; these parameters increased significantly (p < 0.005) over time. In summary, nicotine treatment significantly increased IL-1 alpha concentrations in cultured keratinocytes; however, PGE(2) synthesis was not altered. 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.