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-1beta (IL-1beta) 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 microl) were cultured for 24 hours in supplemented RPMI 1640 alone (control), or in supplemented RPMI 1640 containing 1% ST, 100 microg/ml nicotine, 1 microg/ml Porphyromonas gingivalis LPS, or 1 microg/ml P. gingivalis LPS and either 100 microg/ml nicotine or 1% ST. Enzyme immunoassays were used to quantify PGE2 and IL-1beta. Treatments were compared by repeated measures ANOVA. 100 microg/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 microg/ml nicotine and 1% ST, however, had no effect on IL-1beta secretion by PBMC. Enhanced PGE2 secretion also was seen when PBMC were treated with P. gingivalis LPS+ 100 microg/ml nicotine relative to P. gingivalis LPS alone (p<0.007). In contrast, 100 microg/ml nicotine significantly downregulated IL-1beta 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.

Impairment of human NK cell cytotoxic activity and cytokine release by cigarette smoke

“…It is well known that IL-12 regulates NK cell-mediated IFN-␥ production [25,26,48,49]. In this study, we report for the first time that cigarette smoke blocked IL-12p40 production by poly I:C-activated PBMCs.…”

Regulation of gene expression by tobacco product preparations in cultured human dermal fibroblasts

“…The concentration of STE administered to cells was based on previous studies in which 1% STE was added to cultured cells (Bernzweig et al, 1998; Payne et al, 1994) and reports which indicate that salivary nicotine concentrations in ST users range from 70 to 1560 μg/ml (Petro, 2003; Petro et al, 2002). The low concentration of TPM used in our study was based on previous reports which indicate that nicotine concentrations in unstimulated saliva of smokers range from 0.9 to 4.6 μg/ml (Robson et al, 2010), and data demonstrating that higher concentrations of TPM may be cytotoxic (Gao et al, 2013).…”

Aspectos clínicos, microbiológicos e tratamento periodontal em pacientes fumantes portadores de doença periodontal crônica: revisão da literatura

“…3 Evidências clínicas mostram que fumantes possuem maior perda óssea, maior número de bolsas profundas e são mais susceptíveis ao desenvolvimento de lesões de bifurcação. 4 Entretanto, podem apresentar menor inflamação gengival do que não fumantes. 5 Produtos químicos e toxinas da fumaça do cigarro podem retardar a cicatrização por inibir funções celulares básicas.…”