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A varying T cell subtype explains apparent tobacco smoking induced single CpG hypomethylation in whole blood.

Bauer M, Linsel G, Fink B, Offenberg K, Hahn AM, Sack U, Knaack H, Eszlinger M, Herberth G - Clin Epigenetics (2015)

Bottom Line: Within two independent cohorts, we confirmed the differentially expression of the GPR15 gene when smokers and non-smokers subjects are compared.Treatment of peripheral blood mononuclear cell (PBMC) cultures with aqueous cigarette smoke extract did not induce a higher proportion of this T cell subtype.Our results underline that DNA hypomethylation at cg19859270 site, observed in WBCs of smokers, did not arise by direct effect of tobacco smoking compounds on methylation of DNA but rather by the enrichment of a tobacco-smoking-induced lymphocyte population in the peripheral blood.

View Article: PubMed Central - PubMed

Affiliation: Department of Environmental Immunology, Helmholtz Centre for Environmental Research-UFZ, Leipzig, 04318 Germany.

ABSTRACT

Background: Many recent epigenetic studies report that cigarette smoking reduces DNA methylation in whole blood at the single CpG site cg19859270 within the GPR15 gene.

Results: Within two independent cohorts, we confirmed the differentially expression of the GPR15 gene when smokers and non-smokers subjects are compared. By validating the GPR15 protein expression at the cellular level, we found that the observed decreased methylation at this site in white blood cells (WBC) of smokers is mainly caused by the high proportion of CD3+GPR15+ expressing T cells in peripheral blood. In current smokers, the percentage of GPR15+ cells among CD3+ T cells in peripheral blood is significantly higher (15.5 ± 7.2 %, mean ± standard deviation) compared to non-smokers (3.7 ± 1.6 %). Treatment of peripheral blood mononuclear cell (PBMC) cultures with aqueous cigarette smoke extract did not induce a higher proportion of this T cell subtype.

Conclusions: Our results underline that DNA hypomethylation at cg19859270 site, observed in WBCs of smokers, did not arise by direct effect of tobacco smoking compounds on methylation of DNA but rather by the enrichment of a tobacco-smoking-induced lymphocyte population in the peripheral blood.

No MeSH data available.


Influence of cigarette smoke extract (CSE) on GPR15 expression in PBMCs of randomly selected non-smokers (NS, n = 3) and smokers (S, n = 3). PBMCs were exposed in vitro for 5 days
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Fig5: Influence of cigarette smoke extract (CSE) on GPR15 expression in PBMCs of randomly selected non-smokers (NS, n = 3) and smokers (S, n = 3). PBMCs were exposed in vitro for 5 days

Mentions: To identify any causative role of active cigarette smoking to the excess of GPR15+ cells in blood, we investigated the impact of different CSE concentrations on PBMCs isolated from smokers and non-smokers (Fig. 5). The CSE did not increase the proportion of GPR15-expressing cells.Fig. 5


A varying T cell subtype explains apparent tobacco smoking induced single CpG hypomethylation in whole blood.

Bauer M, Linsel G, Fink B, Offenberg K, Hahn AM, Sack U, Knaack H, Eszlinger M, Herberth G - Clin Epigenetics (2015)

Influence of cigarette smoke extract (CSE) on GPR15 expression in PBMCs of randomly selected non-smokers (NS, n = 3) and smokers (S, n = 3). PBMCs were exposed in vitro for 5 days
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4526203&req=5

Fig5: Influence of cigarette smoke extract (CSE) on GPR15 expression in PBMCs of randomly selected non-smokers (NS, n = 3) and smokers (S, n = 3). PBMCs were exposed in vitro for 5 days
Mentions: To identify any causative role of active cigarette smoking to the excess of GPR15+ cells in blood, we investigated the impact of different CSE concentrations on PBMCs isolated from smokers and non-smokers (Fig. 5). The CSE did not increase the proportion of GPR15-expressing cells.Fig. 5

Bottom Line: Within two independent cohorts, we confirmed the differentially expression of the GPR15 gene when smokers and non-smokers subjects are compared.Treatment of peripheral blood mononuclear cell (PBMC) cultures with aqueous cigarette smoke extract did not induce a higher proportion of this T cell subtype.Our results underline that DNA hypomethylation at cg19859270 site, observed in WBCs of smokers, did not arise by direct effect of tobacco smoking compounds on methylation of DNA but rather by the enrichment of a tobacco-smoking-induced lymphocyte population in the peripheral blood.

View Article: PubMed Central - PubMed

Affiliation: Department of Environmental Immunology, Helmholtz Centre for Environmental Research-UFZ, Leipzig, 04318 Germany.

ABSTRACT

Background: Many recent epigenetic studies report that cigarette smoking reduces DNA methylation in whole blood at the single CpG site cg19859270 within the GPR15 gene.

Results: Within two independent cohorts, we confirmed the differentially expression of the GPR15 gene when smokers and non-smokers subjects are compared. By validating the GPR15 protein expression at the cellular level, we found that the observed decreased methylation at this site in white blood cells (WBC) of smokers is mainly caused by the high proportion of CD3+GPR15+ expressing T cells in peripheral blood. In current smokers, the percentage of GPR15+ cells among CD3+ T cells in peripheral blood is significantly higher (15.5 ± 7.2 %, mean ± standard deviation) compared to non-smokers (3.7 ± 1.6 %). Treatment of peripheral blood mononuclear cell (PBMC) cultures with aqueous cigarette smoke extract did not induce a higher proportion of this T cell subtype.

Conclusions: Our results underline that DNA hypomethylation at cg19859270 site, observed in WBCs of smokers, did not arise by direct effect of tobacco smoking compounds on methylation of DNA but rather by the enrichment of a tobacco-smoking-induced lymphocyte population in the peripheral blood.

No MeSH data available.