Scratching the surface – tobacco-induced bacterial biofilms

Abstract

Individual environmental factors, such as iron, temperature and oxygen, are known to have a profound effect on bacterial phenotype. Therefore, it is surprising so little known is about the influence of chemically complex cigarette smoke on bacterial physiology. Recent evidence has demonstrated that tobacco smoke and components alter the bacterial surface and promote biofilm formation in several important human pathogens, including Staphylococcus aureus, Streptococcus mutans, Klebsiella pneumonia, Porphyromonas gingivalis and Pseudomonas aeruginosa. The mechanisms underlying this phenomenon and the relevance to increased susceptibility to infectious disease in smokers and to treatment are reviewed.

A Comparison of Flavorless Electronic Cigarette-Generated Aerosol and Conventional Cigarette Smoke on the Planktonic Growth of Common Oral Commensal Streptococci

“…Studies based on 16S rRNA analysis show a significant change in the overall microbial profile between smokers and non-smokers, where the former display a much lower diversity index [59,60]. It is important to note that tobacco smoke promotes biofilm growth of oral pathogens, including P. gingivalis, and S. mutans [22,58,[61][62][63][64]. The three commensal species in this study have been shown to arrest the growth of common pathogens [16,17,65].…”

Site‐specific treatment outcome in smokers following non‐surgical and surgical periodontal therapy

“…In perspective, early dysbiosis in subgingival plaque colonization is influenced by cigarette smoke and in a dose responding manner (Hutcherson et al. ). P. gingivalis has a potential to enhance early plaque formation in smokers (Bagaitkar et al.…”

Porphyromonas gingivalis infection in gestational diabetes mellitus and survival in tobacco smokers.

“…Apart from the genes involved in metabolic processes, several genes involved in P. gingivalis attachment to host tissues and other bacterial species were also identified in GAM-CSE model. The genes identified so far are from several studies that have shown increased homotypic and heterotypic biofilm formation by P. gingivalis under the influence of cigarette smoke [157,197,360]. These findings support the idea of increased periodontal pathogen infection in smokers as a result of the dysbiotic influence of P.…”

“…Increased prevalence of the keystone pathogen P. gingivalis, has repeatedly been shown and infection is more persistent in smokers compared with non-smokers [197]. The adoption of 16S ribosomal RNA gene (rDNA) amplification by PCR, followed by cloning and sequencing, has allowed more comprehensive broad-range investigation of oral bacterial communities.…”