The mediating roles of the oral microbiome in saliva and subgingival sites between e-cigarette smoking and gingival inflammation

BMC Microbiology

Research

Hyunwook Koh¹  Ni Zhao²  Hermes Reyes-Caballero³  Michael Patatanian³  Bongsoo Park⁴  Shyam Biswal⁵  Janet T. Holbrook⁶  Jill Meinert⁶  Leah I. Leinbach⁷ 

[1] Department of Applied Mathematics and Statistics, The State University of New York, 21985, Incheon, Korea, South Korea;Department of Biostatistics, Johns Hopkins School of Public Health, 21205, Baltimore, MD, USA;Department of Environmental Health and Engineering, Johns Hopkins School of Public Health, 615 N Wolfe St, 21205, Baltimore, MD, USA;Department of Environmental Health and Engineering, Johns Hopkins School of Public Health, 615 N Wolfe St, 21205, Baltimore, MD, USA;Epigenetics and Stem Cell Aging, Translational Gerontology Branch, National Institute On Aging, National Institute of Health, 21224, Baltimore, MD, USA;Department of Environmental Health and Engineering, Johns Hopkins School of Public Health, 615 N Wolfe St, 21205, Baltimore, MD, USA;Johns Hopkins School of Medicine, 21205, Baltimore, MD, USA;Department of Epidemiology, Johns Hopkins School of Public Health, 21205, Baltimore, MD, USA;Department of Health Policy and Management, Johns Hopkins School of Public Health, 21205, Baltimore, MD, USA;Johns Hopkins School of Medicine, 21205, Baltimore, MD, USA;

关键词: Electronic cigarette;    Oral microbiome;    Saliva microbiome;    Subgingival microbiome;    Gingival inflammation;    Periodontal disease;   

DOI  :  10.1186/s12866-023-02779-z

 received in 2022-07-25, accepted in 2023-01-19,  发布年份 2023

来源: Springer

【 摘 要 】

BackgroundElectronic cigarettes (ECs) have been widely used by young individuals in the U.S. while being considered less harmful than conventional tobacco cigarettes. However, ECs have increasingly been regarded as a health risk, producing detrimental chemicals that may cause, combined with poor oral hygiene, substantial inflammation in gingival and subgingival sites. In this paper, we first report that EC smoking significantly increases the odds of gingival inflammation. Then, through mediation analysis, we seek to identify and explain the mechanism that underlies the relationship between EC smoking and gingival inflammation via the oral microbiome.MethodsWe collected saliva and subgingival samples from 75 EC users and 75 non-users between 18 and 34 years in age and profiled their microbial compositions via 16S rRNA amplicon sequencing. We conducted raw sequence data processing, denoising and taxonomic annotations using QIIME2 based on the expanded human oral microbiome database (eHOMD). We then created functional annotations (i.e., KEGG pathways) using PICRUSt2.ResultsWe found significant increases in α-diversity for EC users and disparities in β-diversity between EC users and non-users. We also found significant disparities between EC users and non-users in the relative abundance of 36 microbial taxa in the saliva site and 71 microbial taxa in the subgingival site. Finally, we found that 1 microbial taxon in the saliva site and 18 microbial taxa in the subgingival site significantly mediated the effects of EC smoking on gingival inflammation. The mediators on the genus level, for example, include Actinomyces, Rothia, Neisseria, and Enterococcus in the subgingival site. In addition, we report significant disparities between EC users and non-users in the relative abundance of 71 KEGG pathways in the subgingival site.ConclusionsThese findings reveal that continued EC use can further increase microbial dysbiosis that may lead to periodontal disease. Our findings also suggest that continued surveillance for the effect of ECs on the oral microbiome and its transmission to oral diseases is needed.

【 授权许可】

CC BY   
© The Author(s) 2023

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