E-cigarette vapor exposure skews competition between colonizing oral Streptococci to allow biofilm formation of S. mutans and activation of stress and survival pathways in the oral cavity.

E-cigarette (e-cig) use is rising, but much is unknown about the effects of its vapor. This vapor contains chemicals such as propylene glycol, a known antimicrobial, and nicotine, whose derivatives are carcinogenic. Here, we study the effects of vaping on resident bacteria of the oral cavity and on oral cell inflammation, which is linked to tumorigenesis. Streptococcus mutans, Streptococcus sanguinis, and Streptococcus gordonii species are significant residents in the oral cavity, with S. mutans the primary cause of dental caries. Growth and biofilm formation is enhanced upon exposure to traditional cigarette smoke in vitro. We aim to analyze the interplay between e-cigarette vapor and oral streptococci colonizing of the oral epithelium. S. mutans, S. sanguinis, and S. gordonii were treated using nicotine-free and 3mg nicotine vapor, as well as double-shot menthol freeze flavored 3mg nicotine vapor in a vape chamber designed to phenocopy physiologically relevant exposure. Next, we analyzed the effects on growth and biofilm formation. Nicotine-independent inhibition of growth occurred upon exposure in all three species. Interestingly, biofilm formation was enhanced in S. mutans while decreased in S. sanguinis and S. gordonii. Upon exposure to the same conditions in the vape chamber, oral epithelial cells showed activation of survival pathways, such as ERK 1/2, by Western blot. Upon coculturing of bacterial and oral epithelial cells at a multiplicity of infection of one for five hours exposed to the same conditions, we observed activation of survival and inflammatory pathways, by Western blot. The pioneer colonizers S. gordonii and S. sanguinis generally antagonize caries-causing S. mutans, which can become a predominant member of the community under appropriate conditions, leading to dental caries formation. The observed decrease in the biofilm formation of the commensals S. sanguinis and S. gordonii upon e-cig vapor exposure indicates the opportunistic colonization of S. mutans, whose biofilm-forming abilities increased. Following e-cig usage, dental caries, periodontitis, and eventually cancer in the oral epithelium may result from this dysbiosis of the microbiome in the oral cavity. Citation Format: Matthew Caldwell, Alma Catala Valentin, Joshua Bernard, Sean Moore, Claudia D. Andl. E-cigarette vapor exposure skews competition between colonizing oral Streptococci to allow biofilm formation of S. mutans and activation of stress and survival pathways in the oral cavity [abstract]. In: Proceedings of the AACR Special Conference on the Microbiome, Viruses, and Cancer; 2020 Feb 21-24; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2020;80(8 Suppl):Abstract nr B03.