The making of a miscreant: tobacco smoke and the creation of pathogen-rich biofilms.
The making of a miscreant: tobacco smoke and the creation of pathogen-rich biofilms.
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DOI：
10.1038/s41522-017-0033-2
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发表时间：
2017
影响因子：
9.2
通讯作者：
Kumar PS
中科院分区：
文献类型：
--
作者：
Shah SA;Ganesan SM;Varadharaj S;Dabdoub SM;Walters JD;Kumar PS
We have previously reported that oral biofilms in clinically healthy smokers are pathogen-rich, and that this enrichment occurs within 24 h of biofilm formation. The present investigation aimed to identify a mechanism by which smoking creates this altered community structure. By combining in vitro microbial–mucosal interface models of commensal (consisting of Streptococcus oralis, Streptococcus sanguis, Streptococcus mitis, Actinomyces naeslundii, Neisseria mucosa and Veillonella parvula) and pathogen-rich (comprising S.oralis, S.sanguis, S.mitis, A.naeslundii, N.mucosa and V.parvula, Fusobacterium nucleatum, Porphyromonas gingivalis, Filifactor alocis, Dialister pneumosintes, Selenonomas sputigena, Selenominas noxia, Catonella morbi, Parvimonas micra and Tannerella forsythia) communities with metatranscriptomics, targeted proteomics and fluorescent microscopy, we demonstrate that smoke exposure significantly downregulates essential metabolic functions within commensal biofilms, while significantly increasing expression of virulence genes, notably lipopolysaccharide (LPS), flagella and capsule synthesis. By contrast, in pathogen-rich biofilms several metabolic pathways were over-expressed in response to smoke exposure. Under smoke-rich conditions, epithelial cells mounted an early and amplified pro-inflammatory and oxidative stress response to these virulence-enhanced commensal biofilms, and a muted early response to pathogen-rich biofilms. Commensal biofilms also demonstrated early and widespread cell death. Similar results were observed when smoke-free epithelial cells were challenged with smoke-conditioned biofilms, but not vice versa. In conclusion, our data suggest that smoke-induced transcriptional shifts in commensal biofilms triggers a florid pro-inflammatory response, leading to early commensal death, which may preclude niche saturation by these beneficial organisms. The cytokine-rich, pro-oxidant, anaerobic environment sustains inflammophilic bacteria, and, in the absence of commensal antagonism, may promote the creation of pathogen-rich biofilms in smokers. Tobacco smoke inhibits the metabolism of beneficial bacteria in biofilms, while activating specific genes in pathogenic bacteria. This suggests a mechanism to explain how smoking quickly leads to the formation of damaging biofilms in the mouth and respiratory tract. Purnima Kumar and colleagues at Ohio State University, USA studied the effect of tobacco smoke on cultured biofilms used to model those that form on mucous membranes. They detected specific and varied changes in the activity of genes, proteins and metabolism that allowed pathogenic bacteria to displace beneficial “commensal” bacteria. The research suggests the transition toward pathogen-rich biofilms may contribute to the health effects of smoking by causing increased inflammation of mucous membranes and the production of damaging oxidant chemicals. Further research should investigate the chemical constituents of smoke responsible for these effects.
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