Potential Suppressive Effect of Nicotine on the Inflammatory Response in Oral Epithelial Cells: An In Vitro Study.

Na An,Xiaohui Rausch-Fan,Marco Aoqi Rausch,Jasmin Holl,Xuekui Wang,Oleh Andrukhov

doi:10.3390/ijerph18020483

Abstract

Smoking is a well-recognized risk factor for oral mucosal and periodontal diseases. Nicotine is an important component of cigarette smoke. This study aims to investigate the impact of nicotine on the viability and inflammatory mediator production of an oral epithelial cell line in the presence of various inflammatory stimuli. Oral epithelial HSC-2 cells were challenged with nicotine (10−8–10−2 M) for 24 h in the presence or absence of Porphyromonas gingivalis lipopolysaccharide (LPS, 1 µg/mL) or tumor necrosis factor (TNF)-α (10−7 M) for 24 h. The cell proliferation/viability was determined by MTT assay. Gene expression of interleukin (IL)-8, intercellular adhesion molecule (ICAM)-1, and β-defensin was assayed by qPCR. The production of IL-8 protein and cell surface expression of ICAM-1 was assessed by ELISA and flow cytometry, respectively. Proliferation/viability of HSC-2 cells was unaffected by nicotine at concentrations up to 10−3 M and inhibited at 10−2 M. Nicotine had no significant effect on the basal expression of IL-8, ICAM-1, and β-defensin. At the same time, it significantly diminished P. gingivalis LPS or the TNF-α-induced expression levels of these factors. Within the limitations of this study, the first evidence was provided in vitro that nicotine probably exerts a suppressive effect on the production of inflammatory mediators and antimicrobial peptides in human oral epithelial cells.

Highlights

Periodontal disease is a complex multifactorial disorder characterized by oral dysbiosis and dysregulated host immune response, the combined effects of which lead to the destruction of tooth-supporting tissue [1,2,3]
Gingivalis LPS nor tumor necrosis factor (TNF)-α had any significant effect on HSC-2 proliferation/viability
Our results strongly suggest that nicotine reduces antimicrobial activity and may allow overgrowth and invasion of potential periodontal pathogens

Summary

Introduction

Periodontal disease is a complex multifactorial disorder characterized by oral dysbiosis and dysregulated host immune response, the combined effects of which lead to the destruction of tooth-supporting tissue [1,2,3]. Porphyromonas gingivalis (P. gingivalis) is a gram-negative anaerobic bacterium that has been considered as a keystone pathogen in periodontitis development and progression [4]. The oral epithelium is the primary physical barrier to infections and is in continuous contact with potentially pathogenic bacterial biofilms in vivo. P. gingivalis is known to influence the structural and functional integrity of gingival epithelium, which results in the disruption of homeostasis and contributes to the progression of periodontal disease [5,6,7]. The oral epithelium produces several factors that are involved in the maintenance of oral health and antibacterial defense. Production of antimicrobial peptides by epithelium plays an essential role in regulating bacterial growth [10]

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