Effects of Smoking on Inflammatory Markers in a Healthy Population as Analyzed via the Gut Microbiota

Abstract

The number of people who smoke has increased in recent years, and the incidence of smoking-related diseases increases annually. This study was conducted to explore whether smoking affects diseases via changes in the gut microbiota. We enrolled 33 smokers and 121 non-smokers. We collected fecal samples from all participants and performed whole-genome sequencing. Smoking significantly affected the gut microbiota. At the phylum through genus levels, the smokers’ microbiotas showed slight changes compared with those of the non-smokers. The α- and β-diversities differed significantly between the smokers and non-smokers, and the smokers’ gut microbiota compositions differed significantly from those of the non-smokers. At the species level, the relative abundances of Ruminococcus gnavus (P=0.00197) and Bacteroides vulgatus (P=0.0468) were significantly greater in the smokers than in the non-smokers, while the relative abundances of Faecalibacterium prausnitzii (P=0.0000052) and Akkermansia muciniphila (P=0.0057) were significantly lower in the smokers. Smoking increases inflammation in the body by inducing an increased abundance of proinflammatory bacteria. Non-smokers had higher abundances of anti-inflammatory microorganisms than did smokers; these microorganisms can produce short-chain fatty acids, which inhibit inflammation.

Impacts of Cigarette Smoking Status on Metabolomic and Gut Microbiota Profile in Male Patients With Coronary Artery Disease: A Multi-Omics Study

“…At the OTU level, a previous study conducted in a healthy population suggested that the smoking-related microbiota composition profile features the increased R. bromii and depleted A. muciniphila and B. nordii, which is in line with our study in CAD smokers (15). We found via intergroup comparison that the OTUs enriched in current smokers comprise several opportunistic pathogens such as H. parainfluenzae and Klebsiella sp.…”

“…It was reported that Desulfovibrio DNA progressively increased with the smoking burden (pack-years) (26). The overall decreased Veillonella abundance in smokers at the genus level is in line with an earlier study (15). Manhattan plots showed the contributions of differentially abundant OTUs at the class level (Figure 1C).…”

“…Cigarette smoking may influence host microbiota through various mechanisms including upregulating oxidative stressassociated enzymes in gut immune cells, altering the gut mucin layer, and increasing the intestinal pH (12)(13)(14). A prior study showed that gut microbiome compositions of smokers differed significantly from those of never smokers in the healthy population (15), but whether this change can be reversed by smoking cessation remains a matter of controversy (16,17). Besides, the smoking-induced intestinal microbiota changes under the background of chronic diseases like Crohn's disease and ankylosing spondylitis have been investigated but whether this change contributes to disease progression is not determined (18,19).…”

Chronic Systemic Low-Grade Inflammation and Modern Lifestyle: The Dark Role of Gut Microbiota on Related Diseases with a Focus on COVID-19 Pandemic

“…Interestingly, smoking cessation induces only a minor change in microbiota after 12 weeks in ex-smokers, while other research shows a shift after 9 weeks with an increase of Firmicutes and Actinobacteria and a decrease in Bacteroidetes and Proteobacteria [245]. The reduction of anti-inflammatory bacteria such as F. prausnitzii and Akkermansia muciniphila with a higher abundance of pro-inflammatory bacteria such as Ruminococcus gnavus and Bacteroides vulgatus, as revealed by a metagenomic sequencing, can explain the systemic pro-inflammatory action of smoke [246].…”

Correlation between nicotine dependence and inflammatory biomarkers in Thai smokers: Eight weeks of synbiotic intervention

“…LPS is a protein present on the outer surface of gram-negative bacteria. Generally, its target is TLR-4, which delivers the action on different receptors [15]- [17]. Human immune cells recognize extracellular LPS through the Tolllike receptor-4 (TLR-4).…”