2021
DOI: 10.3390/ijerph18020483
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Potential Suppressive Effect of Nicotine on the Inflammatory Response in Oral Epithelial Cells: An In Vitro Study

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… Show more

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Cited by 12 publications
(3 citation statements)
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“…Nicotine is a common ingredient in tobacco and e-cigarettes, and it is present in tobacco and most e-cigarettes. Studies have shown that nicotine may inhibit the production of inflammatory factors in oral epithelial cells, while other studies have shown that nicotine can also be produce cytotoxicity to human periodontal cells and induce human periodontal cells to produce IL-1β and IL-8 . E-cigarettes are cytotoxic to a variety of cells, including gingival fibroblasts, gingival mesenchymal stem cells, and gingival epithelial cells, and affect cell proliferation, but e-cigarettes have less effect on cell proliferation and viability than tobacco .…”
Section: Discussionmentioning
confidence: 99%
“…Nicotine is a common ingredient in tobacco and e-cigarettes, and it is present in tobacco and most e-cigarettes. Studies have shown that nicotine may inhibit the production of inflammatory factors in oral epithelial cells, while other studies have shown that nicotine can also be produce cytotoxicity to human periodontal cells and induce human periodontal cells to produce IL-1β and IL-8 . E-cigarettes are cytotoxic to a variety of cells, including gingival fibroblasts, gingival mesenchymal stem cells, and gingival epithelial cells, and affect cell proliferation, but e-cigarettes have less effect on cell proliferation and viability than tobacco .…”
Section: Discussionmentioning
confidence: 99%
“…Nicotine inhibited the expression of β-defensin. Nicotine may have an inhibitory effect on the production of inflammatory factors in oral epithelial cells [9]. Studies have shown that nicotine also restrains the proliferation and cell cycle of human periodontal ligament cells by upregulating miR-30a expression and downregulating cell cycle protein E2 expression, thereby disrupting the regeneration of periodontal tissue [10].…”
Section: Composition Analysis Of Electronic Cigarettes and Traditiona...mentioning
confidence: 99%
“…Using microarrays representative of the P. gingivalis genome, it is revealed that CSE-exposure resulted in differential regulation of 6.8% of P. gingivalis genes, including detoxification and oxidative stress-related genes, DNA repair genes and multiple genes related to P. gingivalis virulence [ 61 ]. More studies demonstrated the multiple regulatory effects of smoking on expression or function of virulence factors of P. gingivalis , including the long fimbriae FimA [ 52 , 61 ], capsular polysaccharides [ 52 ], outer membrane proteins RagA and RagB [ 61 ], Kgp and Rgp gingipain [ 62 ] and LPS [ 63 ] ( Figure 1 ).…”
Section: Impact Of Smoking On Pathogenicity Of Periodontopathogensmentioning
confidence: 99%