Interleukin-1 and interleukin-8 in nicotine- and lipopolysaccharide-exposed gingival keratinocyte cultures

G K Johnson; J M Guthmiller; S Joly; C C Organ; D V Dawson

doi:10.1111/j.1600-0765.2009.01262.x

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Interleukin-1 and interleukin-8 in nicotine- and lipopolysaccharide-exposed gingival keratinocyte cultures

Journal article

Peer reviewed

Interleukin-1 and interleukin-8 in nicotine- and lipopolysaccharide-exposed gingival keratinocyte cultures

G K Johnson, J M Guthmiller, S Joly, C C Organ and D V Dawson

Journal of periodontal research, Vol.45(4), pp.583-588

08/2010

DOI: 10.1111/j.1600-0765.2009.01262.x

PMID: 20337880

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Abstract

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-1 alpha (IL-1 alpha) and interleukin-8 (IL-8). Gingival keratinocyte cultures were established from 10 healthy, non-tobacco-using subjects. The cells were stimulated for 24 h with 1 mum or 1 mm nicotine and/or 10 microg/mL Escherichia coli or Porphyromonas gingivalis LPS. Interleukin-1 alpha and IL-8 proteins were quantified using ELISAs. Compared with untreated cultures, 1 mm nicotine stimulated production of IL-1 alpha (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-1 alpha 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 mum 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. 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.

Cell Survival - drug effects

Gingiva - immunology

Interleukin-1alpha - analysis

Humans

Cells, Cultured

Porphyromonas gingivalis - physiology

Interleukin-8 - analysis

Keratinocytes - immunology

Nicotine - pharmacology

Drug Synergism

Gingiva - drug effects

Keratinocytes - drug effects

Time Factors

Inflammation Mediators - pharmacology

Gingiva - cytology

Lipopolysaccharides - pharmacology

Escherichia coli - physiology

Nicotinic Agonists - pharmacology

Details

Title: Subtitle: Interleukin-1 and interleukin-8 in nicotine- and lipopolysaccharide-exposed gingival keratinocyte cultures
Creators: G K Johnson - Department of Periodontics, University of Iowa College of Dentistry, Iowa City, IA 52242-1001, USA. georgia-johnson@uiowa.edu
J M Guthmiller
S Joly
C C Organ
D V Dawson
Resource Type: Journal article
Publication Details: Journal of periodontal research, Vol.45(4), pp.583-588
Publisher: United States
DOI: 10.1111/j.1600-0765.2009.01262.x
PMID: 20337880
ISSN: 0022-3484
eISSN: 1600-0765
Grant note: R29DEO10153 / PHS HHS R01 DE13334 / NIDCR NIH HHS
Language: English
Date published: 08/2010
Academic Unit: Biostatistics; Pediatric Dentistry; Periodontics
Record Identifier: 9984065714702771

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