Nicotine and Smokeless Tobacco effects on gingival and Peripheral Blood Mononuclear Cells

Eric Bernzweig, Jeffrey B Payne, Richard A Reinhardt, John K. Dyer, Kashinath D. Patil

Research output: Contribution to journalArticle

46 Citations (Scopus)

Abstract

The pathogenesis of tobacco-related periodontal diseases is not well understood. The purpose of this study was therefore to investigate smokeless tobacco extract (ST) and nicotine effects on prostaglandin E2 (PGE2) and interleukin-1β (IL-1β) secretion by peripheral blood mononuclear cells (PBMC, consisting of monocytes and lymphocytes) and gingival mononuclear cells (GMC). Both peripheral blood and gingival tissue adjacent to the alveolar crest were taken from non-smoking adult periodontitis patients. Gingival tissue was treated with collagenase and deoxyribonuclease and GMC and PBMC were isolated by Ficoll-Hypaque centrifugation. GMC and PBMC (100,000 cells/200 μl) were cultured for 24 hours in supplemented RPMI 1640 alone (control), or in supplemented RPMI 1640 containing 1% ST, 100 μg/ml nicotine, 1 μg/ml Porphyromonas gingivalis LPS, or 1 μg/ml P. gingivalis LPS and either 100 μg/ml nicotine or 1% ST. Enzyme immunoassays were used to quantify PGE2 and IL-1β. Treatments were compared by repeated measures ANOVA. 100 μg/ml nicotine (7-fold, p<0.02) and 1% ST (3.5-fold, p<0.004) significantly increased secretion of PGE2 by PBMC relative to control cultures. 100 μg/ml nicotine and 1% ST, however, had no effect on IL-1β secretion by PBMC. Enhanced PGE2 secretion also was seen when PBMC were treated with P. gingivalis LPS+100 μg/ml nicotine relative to P. gingivalis LPS alone (p<0.007). In contrast, 100 μg/ml nicotine significantly downregulated IL-1β secretion by GMC relative to medium alone (p<0.008) and had no effect on PGE2 secretion by GMC. These data indicate that while nicotine and ST can stimulate PBMC to secrete PGE2, they cannot activate further mononuclear cells extracted from gingiva, possibly due to maximal previous stimulation in the periodontitis lesion.

Original languageEnglish (US)
Pages (from-to)246-252
Number of pages7
JournalJournal of Clinical Periodontology
Volume25
Issue number3
DOIs
StatePublished - Jan 1 1998

Fingerprint

Smokeless Tobacco
Nicotine
Blood Cells
Dinoprostone
Porphyromonas gingivalis
Interleukin-1
Diatrizoate
Chronic Periodontitis
Ficoll
Deoxyribonucleases
Periodontitis
Gingiva
Periodontal Diseases
Collagenases
Immunoenzyme Techniques
Centrifugation
Tobacco
Monocytes
Analysis of Variance
Down-Regulation

Keywords

  • Mononuclear cell
  • Nicotine
  • Periodontitis
  • Smokeless tobacco

ASJC Scopus subject areas

  • Periodontics

Cite this

Nicotine and Smokeless Tobacco effects on gingival and Peripheral Blood Mononuclear Cells. / Bernzweig, Eric; Payne, Jeffrey B; Reinhardt, Richard A; Dyer, John K.; Patil, Kashinath D.

In: Journal of Clinical Periodontology, Vol. 25, No. 3, 01.01.1998, p. 246-252.

Research output: Contribution to journalArticle

@article{3cdf9d7006254f15a38a66c0b040cb5a,
title = "Nicotine and Smokeless Tobacco effects on gingival and Peripheral Blood Mononuclear Cells",
abstract = "The pathogenesis of tobacco-related periodontal diseases is not well understood. The purpose of this study was therefore to investigate smokeless tobacco extract (ST) and nicotine effects on prostaglandin E2 (PGE2) and interleukin-1β (IL-1β) secretion by peripheral blood mononuclear cells (PBMC, consisting of monocytes and lymphocytes) and gingival mononuclear cells (GMC). Both peripheral blood and gingival tissue adjacent to the alveolar crest were taken from non-smoking adult periodontitis patients. Gingival tissue was treated with collagenase and deoxyribonuclease and GMC and PBMC were isolated by Ficoll-Hypaque centrifugation. GMC and PBMC (100,000 cells/200 μl) were cultured for 24 hours in supplemented RPMI 1640 alone (control), or in supplemented RPMI 1640 containing 1{\%} ST, 100 μg/ml nicotine, 1 μg/ml Porphyromonas gingivalis LPS, or 1 μg/ml P. gingivalis LPS and either 100 μg/ml nicotine or 1{\%} ST. Enzyme immunoassays were used to quantify PGE2 and IL-1β. Treatments were compared by repeated measures ANOVA. 100 μg/ml nicotine (7-fold, p<0.02) and 1{\%} ST (3.5-fold, p<0.004) significantly increased secretion of PGE2 by PBMC relative to control cultures. 100 μg/ml nicotine and 1{\%} ST, however, had no effect on IL-1β secretion by PBMC. Enhanced PGE2 secretion also was seen when PBMC were treated with P. gingivalis LPS+100 μg/ml nicotine relative to P. gingivalis LPS alone (p<0.007). In contrast, 100 μg/ml nicotine significantly downregulated IL-1β secretion by GMC relative to medium alone (p<0.008) and had no effect on PGE2 secretion by GMC. These data indicate that while nicotine and ST can stimulate PBMC to secrete PGE2, they cannot activate further mononuclear cells extracted from gingiva, possibly due to maximal previous stimulation in the periodontitis lesion.",
keywords = "Mononuclear cell, Nicotine, Periodontitis, Smokeless tobacco",
author = "Eric Bernzweig and Payne, {Jeffrey B} and Reinhardt, {Richard A} and Dyer, {John K.} and Patil, {Kashinath D.}",
year = "1998",
month = "1",
day = "1",
doi = "10.1111/j.1600-051X.1998.tb02435.x",
language = "English (US)",
volume = "25",
pages = "246--252",
journal = "Journal of Clinical Periodontology",
issn = "0303-6979",
publisher = "Blackwell Munksgaard",
number = "3",

}

TY - JOUR

T1 - Nicotine and Smokeless Tobacco effects on gingival and Peripheral Blood Mononuclear Cells

AU - Bernzweig, Eric

AU - Payne, Jeffrey B

AU - Reinhardt, Richard A

AU - Dyer, John K.

AU - Patil, Kashinath D.

PY - 1998/1/1

Y1 - 1998/1/1

N2 - The pathogenesis of tobacco-related periodontal diseases is not well understood. The purpose of this study was therefore to investigate smokeless tobacco extract (ST) and nicotine effects on prostaglandin E2 (PGE2) and interleukin-1β (IL-1β) secretion by peripheral blood mononuclear cells (PBMC, consisting of monocytes and lymphocytes) and gingival mononuclear cells (GMC). Both peripheral blood and gingival tissue adjacent to the alveolar crest were taken from non-smoking adult periodontitis patients. Gingival tissue was treated with collagenase and deoxyribonuclease and GMC and PBMC were isolated by Ficoll-Hypaque centrifugation. GMC and PBMC (100,000 cells/200 μl) were cultured for 24 hours in supplemented RPMI 1640 alone (control), or in supplemented RPMI 1640 containing 1% ST, 100 μg/ml nicotine, 1 μg/ml Porphyromonas gingivalis LPS, or 1 μg/ml P. gingivalis LPS and either 100 μg/ml nicotine or 1% ST. Enzyme immunoassays were used to quantify PGE2 and IL-1β. Treatments were compared by repeated measures ANOVA. 100 μg/ml nicotine (7-fold, p<0.02) and 1% ST (3.5-fold, p<0.004) significantly increased secretion of PGE2 by PBMC relative to control cultures. 100 μg/ml nicotine and 1% ST, however, had no effect on IL-1β secretion by PBMC. Enhanced PGE2 secretion also was seen when PBMC were treated with P. gingivalis LPS+100 μg/ml nicotine relative to P. gingivalis LPS alone (p<0.007). In contrast, 100 μg/ml nicotine significantly downregulated IL-1β secretion by GMC relative to medium alone (p<0.008) and had no effect on PGE2 secretion by GMC. These data indicate that while nicotine and ST can stimulate PBMC to secrete PGE2, they cannot activate further mononuclear cells extracted from gingiva, possibly due to maximal previous stimulation in the periodontitis lesion.

AB - The pathogenesis of tobacco-related periodontal diseases is not well understood. The purpose of this study was therefore to investigate smokeless tobacco extract (ST) and nicotine effects on prostaglandin E2 (PGE2) and interleukin-1β (IL-1β) secretion by peripheral blood mononuclear cells (PBMC, consisting of monocytes and lymphocytes) and gingival mononuclear cells (GMC). Both peripheral blood and gingival tissue adjacent to the alveolar crest were taken from non-smoking adult periodontitis patients. Gingival tissue was treated with collagenase and deoxyribonuclease and GMC and PBMC were isolated by Ficoll-Hypaque centrifugation. GMC and PBMC (100,000 cells/200 μl) were cultured for 24 hours in supplemented RPMI 1640 alone (control), or in supplemented RPMI 1640 containing 1% ST, 100 μg/ml nicotine, 1 μg/ml Porphyromonas gingivalis LPS, or 1 μg/ml P. gingivalis LPS and either 100 μg/ml nicotine or 1% ST. Enzyme immunoassays were used to quantify PGE2 and IL-1β. Treatments were compared by repeated measures ANOVA. 100 μg/ml nicotine (7-fold, p<0.02) and 1% ST (3.5-fold, p<0.004) significantly increased secretion of PGE2 by PBMC relative to control cultures. 100 μg/ml nicotine and 1% ST, however, had no effect on IL-1β secretion by PBMC. Enhanced PGE2 secretion also was seen when PBMC were treated with P. gingivalis LPS+100 μg/ml nicotine relative to P. gingivalis LPS alone (p<0.007). In contrast, 100 μg/ml nicotine significantly downregulated IL-1β secretion by GMC relative to medium alone (p<0.008) and had no effect on PGE2 secretion by GMC. These data indicate that while nicotine and ST can stimulate PBMC to secrete PGE2, they cannot activate further mononuclear cells extracted from gingiva, possibly due to maximal previous stimulation in the periodontitis lesion.

KW - Mononuclear cell

KW - Nicotine

KW - Periodontitis

KW - Smokeless tobacco

UR - http://www.scopus.com/inward/record.url?scp=0032010749&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0032010749&partnerID=8YFLogxK

U2 - 10.1111/j.1600-051X.1998.tb02435.x

DO - 10.1111/j.1600-051X.1998.tb02435.x

M3 - Article

C2 - 9543195

AN - SCOPUS:0032010749

VL - 25

SP - 246

EP - 252

JO - Journal of Clinical Periodontology

JF - Journal of Clinical Periodontology

SN - 0303-6979

IS - 3

ER -