Interleukin‐1 and interleukin‐8 in nicotine‐ and lipopolysaccharide‐exposed gingival keratinocyte cultures |
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| Authors: | G K Johnson J M Guthmiller S Joly C C Organ D V Dawson |
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| Institution: | 1. Department of Periodontics, University of Iowa College of Dentistry, Iowa City, IA, USA;2. Dows Institute for Dental Research, University of Iowa College of Dentistry, Iowa City, IA, USA;3. Department of Periodontics, University of North Carolina at Chapel Hill, NC, USA and;4. Department of Preventive and Community Dentistry, University of Iowa College of Dentistry, Iowa City, IA, USA |
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| Abstract: | Johnson GK, Guthmiller JM, Joly S, Organ CC, Dawson DV. Interleukin‐1 and interleukin‐8 in nicotine‐ and lipopolysaccharide‐exposed gingival keratinocyte cultures. J Periodont Res 2010; 45: 583–588. © 2010 John Wiley & Sons A/S Background and Objective: Tobacco use is associated with increased periodontal destruction in both cigarette smokers and smokeless tobacco users. Gingival keratinocytes are the first cells in contact with microbial and tobacco components and play a key role in the innate immune response to these agents. The objective of this study was to evaluate the effect of nicotine and bacterial lipopolysaccharide (LPS) alone and in combination on gingival keratinocyte production of interleukin‐1α (IL‐1α) and interleukin‐8 (IL‐8). Material and Methods: Gingival keratinocyte cultures were established from 10 healthy, non‐tobacco‐using subjects. The cells were stimulated for 24 h with 1 μm or 1 mm nicotine and/or 10 μg/mL Escherichia coli or Porphyromonas gingivalis LPS. Interleukin‐1α and IL‐8 proteins were quantified using ELISAs. Results: Compared with untreated cultures, 1 mm nicotine stimulated production of IL‐1α (p < 0.001); E. coli and P. gingivalis LPS increased IL‐8 production (p = 0.0014 and p = 0.0232, respectively). A combination of nicotine and LPS produced the highest cytokine quantities. Amounts of IL‐1α and IL‐8 following 1 mm nicotine and LPS exposure were significantly greater than in untreated cultures (p < 0.001). Interleukin‐8 was also responsive to 0.1 μm nicotine combined with E. coli or P. gingivalis LPS compared with control cultures (p < 0.0001 and p = 0.0029, respectively). Both cytokines tended to be elevated following the combined treatment relative to nicotine or LPS treatment alone. Conclusion: These results demonstrate that nicotine and LPS differentially regulate IL‐1 and IL‐8 production by gingival keratinocytes. Combined treatment tended to elevate cytokine production further, which may have implications for the progression of periodontitis in tobacco users. |
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| Keywords: | smoking cytokine gingiva in vitro model |
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