Abstract B02: E-cigarette vape and cigarette smoke potentially increase S. aureus oral colonization and inflammatory epithelial signaling
Authors: Catala-Valentin Alma R. , Caldwell Matthew , Cole Alexander M. , Moore Sean , Andl Claudia 
Published: December 2020

Abstract
E-cigarette (E-cig) vaping has gained popularity among middle and high-school students within the last decade, being advertised as a safer alternative to cigarette smoke. While acute lung illness has been reported, it is too early to have epidemiologic data suggesting a role of E-cig on oral squamous cell carcinoma. However, recent studies point to its potentially adverse effects on the human epithelium and the oral human microbial flora. Staphylococcus aureus is a resident of the oral microbiota and its carriage has been shown to be significantly higher in the periodontal pocket of patients with actively progressing periodontitis, which is a chronic inflammatory disease and known precursor for oral squamous cell carcinoma (OSCC). Additionally, S. aureus has also been isolated from OSCC tissues. In this study, we aim to identify the response of S. aureus and the oral epithelium to E-cig vape exposure and, further, to determine the effect of E-cig vape on the interaction of S. aureus with the oral epithelium. To measure differences in the ability to form biofilm upon E-cig vape exposure with (3mg/mL) and without nicotine, we analyzed two clinical S. aureus strains isolated from healthy individuals following a 30s puff delivery and a 5-minute incubation. We observed that E-cig vape induced significantly higher biofilm formation than control air exposure in a specifically designed vape chamber regardless of nicotine content (p&lt;0.01). Furthermore, S. aureus strain obtained from cigarette smokers had a significantly higher attachment capacity to oral epithelial cells than sequence-type matched strains from healthy controls (p&lt;0.05), suggesting an augmented potential for oral colonization upon E-cig vape and cigarette smoke exposure. Oral epithelial cells, when exposed to E-cig vape alone, showed a proinflammatory response, through an increase in COX2, TNFα, and IL8 gene expression by qRT-PCR. Additionally, we observed that E-cig vape induced an increase in the DNA damage marker, p-H2A.X, seen by immunofluorescence staining. E-cig vape and S. aureus exposure induced inflammatory signaling as demonstrated by qRT-PCR for COX2 and TNFα, and nuclear translocation of NF-KB seen by immunofluorescence staining. Furthermore, we observed an epithelial stress response through p-ERK1/2 signaling activation by Western blot. Our research suggests that E-cig exposure could be supporting increased oral carriage of S. aureus, therefore perpetuating an inflammatory response and causing extended DNA damage, which could eventually initiate OSCC.
Citation Format: Alma R. Catala-Valentin, Matthew Caldwell, Alexander M. Cole, Sean Moore, Claudia Andl. E-cigarette vape and cigarette smoke potentially increase S. aureus oral colonization and inflammatory epithelial signaling [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 B02.