Abstract

ABSTRACT Rothia mucilaginosa has been found at high abundance on oral leukoplakia (OLK). The ability of clinical isolates to produce acetaldehyde (ACH) from ethanol has not been investigated. The objective of the current study was to determine the capacity of R. mucilaginosa isolates recovered from OLK to generate ACH. Analysis of R. mucilaginosa genomes (n = 70) shows that this species does not normally encode acetaldehyde dehydrogenase (ALDH) required for detoxification of ACH. The predicted OLK metagenome also exhibited reduced ALDH coding capacity. We analysed ACH production in 8 isolates of R. mucilaginosa and showed that this species is capable of generating ACH in the presence of ethanol. The levels of ACH produced (mean = 53 µM) were comparable to those produced by Neisseria mucosa and Candida albicans in parallel assays. These levels were demonstrated to induce oxidative stress in cultured oral keratinocytes. This study shows that R. mucilaginosa can generate ACH from ethanol in vitro at levels which can induce oxidative stress. This organism likely contributes to oral ACH levels following alcohol consumption and the significance of the increased abundance of R. mucilaginosa in patients with potentially malignant disorders requires further investigation.

Highlights

  • Recent studies have linked changes in the oral microbiome with the development of oral cancers, including oral squamous cell carcinoma (OSCC) [1,2]

  • We recently investigated the microbiome associated with oral leukoplakia (OLK), a potentially malignant lesion with the potential to transform to OSCC

  • These studies identified increased levels of R. mucilaginosa on OLK. This was surprising as previous studies of OSCC have shown that the abundance R. mucilaginosa is decreased at oral cancers [1,38]

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Summary

Introduction

Recent studies have linked changes in the oral microbiome with the development of oral cancers, including oral squamous cell carcinoma (OSCC) [1,2]. Alcohol consumption is a known risk factor for OSCC, ethanol itself is not carcinogenic. Studies have shown that the oral microbiome plays a role in generating ACH in the oral cavity following alcohol consumption [5,11]. In vitro studies have shown that incubation of saliva with ethanol results in the generation of ACH and that saliva from smokers, alcohol drinkers and those with poor oral hygiene generate higher levels of ACH in vitro [11,12,13]. Patients with OSCC and oral lichenoid disease have been shown to harbor acetaldehyde generating microorganisms at lesional sites, and that cultures from smokers generated greater levels of acetaldehyde compared to non-smokers [14]

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