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Article

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

1
Department of General Dentistry II, Peking University School and Hospital of Stomatology, Beijing 100081, China
2
Competence Center for Periodontal Research, University Clinic of Dentistry, Medical University of Vienna, 1090 Vienna, Austria
3
Department of Periodontology, Peking University School and Hospital of Stomatology, Beijing 100081, China
*
Author to whom correspondence should be addressed.
Int. J. Environ. Res. Public Health 2021, 18(2), 483; https://doi.org/10.3390/ijerph18020483
Received: 2 November 2020 / Revised: 18 December 2020 / Accepted: 4 January 2021 / Published: 9 January 2021
(This article belongs to the Special Issue Influence of Risk Factors on Periodontitis and Periodontal Treatment)
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. View Full-Text
Keywords: nicotine; epithelial cell; inflammation; lipopolysaccharide nicotine; epithelial cell; inflammation; lipopolysaccharide
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MDPI and ACS Style

An, N.; Holl, J.; Wang, X.; Rausch, M.A.; Andrukhov, O.; Rausch-Fan, X. Potential Suppressive Effect of Nicotine on the Inflammatory Response in Oral Epithelial Cells: An In Vitro Study. Int. J. Environ. Res. Public Health 2021, 18, 483. https://doi.org/10.3390/ijerph18020483

AMA Style

An N, Holl J, Wang X, Rausch MA, Andrukhov O, Rausch-Fan X. Potential Suppressive Effect of Nicotine on the Inflammatory Response in Oral Epithelial Cells: An In Vitro Study. International Journal of Environmental Research and Public Health. 2021; 18(2):483. https://doi.org/10.3390/ijerph18020483

Chicago/Turabian Style

An, Na, Jasmin Holl, Xuekui Wang, Marco A. Rausch, Oleh Andrukhov, and Xiaohui Rausch-Fan. 2021. "Potential Suppressive Effect of Nicotine on the Inflammatory Response in Oral Epithelial Cells: An In Vitro Study" International Journal of Environmental Research and Public Health 18, no. 2: 483. https://doi.org/10.3390/ijerph18020483

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