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Prostaglandin E 2 and interleukin‐1 concentrations in nicotine‐exposed oral keratinocyte cultures
Author(s) -
Johnson G. K.,
Organ C. C.
Publication year - 1997
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.1997.tb00557.x
Subject(s) - prostaglandin e2 , nicotine , keratinocyte , interleukin , alpha (finance) , interleukin 8 , andrology , cytokine , cell culture , chemistry , prostaglandin , endocrinology , medicine , pharmacology , in vitro , immunology , biology , biochemistry , surgery , construct validity , genetics , patient satisfaction
Oral keratinocytes are the first cells in contact with tobacco components and are capable of producing various inflammatory mediators, including PGE2 and IL‐1. The purpose of this study was to examine PGE2 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 μ m , 10 μ m or 1 mM nicotine for 4, 24 or 48 h. Using enzyme‐linked immunosorbent assays, PGE 2 and IL‐1α were quantified in culture supernatants; IL‐1 α and β 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 PGE2 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 α concentrations in lysates from 1 mM nicotine‐exposed cells were significantly (p < 0.01) greater than those for all other treatments. Interleukin‐1α quantities also declined significantly (p=0.037) over time in the cultures. Interleukin‐1β 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 a 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.