Abstract
BackgroundRecent studies break with traditional opinion that the lower respiratory tract is sterile, and increasingly focus on the lung microbiome and disease. Smoking, as an important etiology of inflammatory lung disease, was considered as a factor influencing lung microbiome variations in our study, and we aimed to study the effect of smoking on inflammation and microbial diversity and community.MethodsForty male mice were selected and randomly divided into a smoking and a non-smoking group. Mice in the smoking group were exposed to smoke smog for 2 h/day for 90 days. Blood and lung tissues were obtained after the experiment, and ELISA was used to measure interleukin-6 and C reactive protein concentrations. 16S rRNA gene quantification and sequencing technology were used to compare microbial diversity and community between the two groups. SAS 9.1 and R software were used to analyze the data.ResultsThirty-six mice survived, and the weight of the smoking group increased more slowly than that of the non-smoking group. Denser inflammation and congestion were observed in the lungs of the smoking mice compared with the non-smoking group Higher microbial diversity was observed in the smoking group, and Enterobacter, Acidimicrobiales_norank, and Caulobacteraceae_Unclassified genus were significantly more abundant in the non-smoking group (P < 0.001).ConclusionsSmoking altered microbial diversities and communities in the lower respiratory tract of mice. Microbial variation should be considered in future studies focusing on smoking-induced inflammatory disease.
Highlights
Recent studies break with traditional opinion that the lower respiratory tract is sterile, and increasingly focus on the lung microbiome and disease
Body weights and survival Four mice died during the experiment
Our study aimed to deepen the understanding of the relationship between smoking, inflammation, and the lower respiratory tract (LRT) microbiome that underlies many of these pathologies
Summary
Recent studies break with traditional opinion that the lower respiratory tract is sterile, and increasingly focus on the lung microbiome and disease. The lower respiratory tract (LRT) was considered sterile because culture-based techniques failed to detect microbes in the LRT [1,2,3] This opinion was changed by recent detection of bacteria in the LRT by newly developed molecular techniques, the widely used high-throughput sequencing of amplicons of the 16S rRNA gene [4, 5]. Markus Hilty et al [7] described a characteristic microbial flora in the bronchial tree that was strikingly distinct between healthy and asthmatic individuals. These findings were milestones in the path to appreciation of the LRT microbiome. It is widely understood to be associated with lung cancer (LC), asthma, chronic obstructive pulmonary disease (COPD), hearing loss, tooth loss, cardiovascular disease, and periodontal disease
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