Background: The microbiota plays a critical role in the process of human carcinogenesis. Pancreatic head carcinoma (PHC)-associated tongue coating microbiome dysbiosis has not yet been clearly defined.Objective: Our aim is to reveal the bacterial composition shifts in the microbiota of the tongue coat of PHC patients.Design: The tongue coating microbiota was analyzed in 30 PHC patients and 25 healthy controls using 16S rRNA gene sequencing technology.Results: The microbiome diversity of the tongue coat in PHC patients was significantly increased, as shown by the Shannon, Simpson, inverse Simpson, Obs and incidence-based coverage estimators. Principal component analysis revealed that PHC patients were colonized by remarkably different tongue coating microbiota than healthy controls and liver cancer patients. Linear discriminant analysis effect size revealed that Leptotrichia, Fusobacterium,Rothia, Actinomyces, Corynebacterium, Atopobium, Peptostreptococcus, Catonella, Oribacterium, Filifactor, Campylobacter, Moraxella and Tannerella were overrepresented in the tongue coating of PHC patients, and Haemophilus, Porphyromonas and Paraprevotella were enriched in the tongue coating microbiota of healthy controls. Strikingly, Haemophilus, Porphyromonas, Leptotrichia and Fusobacterium could distinguish PHC patients from healthy subjects, and Streptococcus and SR1 could distinguish PHC patients from liver cancer patients. Conclusions: These findings identified the microbiota dysbiosis of the tongue coat in PHC patients, and provide insight into the association between the human microbiome and pancreatic cancer.

The gut microbiota is crucial in the pathogenesis of obesity. Abdominal obesity is known to significantly increase the risk of metabolic syndrome and cardiovascular disease, so further study is needed to investigate the changes of intestinal microorganisms in patients with excessive visceral fat. In our study, 41 people (n = 41) with normal body mass index (BMI) (18.5 ≤ BMI < 23.9) were included and divided into the low visceral fat area (L-VFA) group (n = 23, VFA < 100 cm²) and the high visceral fat area (H-VFA) group (n = 18, VFA ≥ 100 cm²). Several clinical indicators of the H-VFA group were significantly higher than those of the L-VFA group, including the waist circumference (WC), the fasting blood glucose (FBG), the triglyceride (TG), the total cholesterol (TC), the low-density lipoprotein cholesterol (LDL), the serum uric acid (SUA), the white blood cell count (WBC), the blood neutrophil count (NEC), and the blood lymphocyte count (LYC). Using whole-genome shotgun sequencing, we found that the types of the intestinal microbiota of H-VFA patients were different from those of the L-VFA patients, with 18 bacteria enriched in the H-VFA group and nine bacteria in the L-VFA group. A total of 16 species of gut microbes showed a strong correlation with VFA, and Escherichia coli has the strongest correlation, followed by Mitsuokella unclassified, Bifidobacterium longum, Escherichia unclassified, Ruminococcus torques, Dialister succinatiphilus, Eubacterium hallii, and Ruminococcus gnavus. Compared to the VFA, only two species show a strong correlation with BMI and WC. Further functional genetic studies suggested that the degradation of short-chain fatty acids (SCFAs) and the generation of lipopolysaccharide (LPS) might be related to visceral fat accumulation. Together, visceral fat was more closely correlated with the gut microbiome compared with BMI and WC. It suggested an intrinsic connection between the gut microbiome and visceral fat and its related metabolic disorders. Specific microbial species and pathways associated with visceral fat accumulation might contribute to new targeted therapies for visceral fat and its metabolic disorders.

Carotid atherosclerosis (CAS) is a reflection of systemic atherosclerosis and the main pathological processes of cardiovascular disease (CVD), namely, carotid intima–media thickening, carotid plaque formation, and carotid stenosis. Accumulating evidence indicates that the gut microbiota plays an important role in CVD and gut–brain disorders, but the associations of the composition and metabolites of the gut microbiome with CAS have not been studied comprehensively. We performed a gut microbiome genome-wide association study in 31 patients with CAS and 51 healthy controls using whole-genome shotgun sequencing. We found that several risk factors (waist circumference, body mass index, diastolic blood pressure, systolic blood pressure, fasting blood glucose, glycated hemoglobin A1c, total cholesterol, triglyceride, and low-density lipoprotein cholesterol) and inflammatory markers (white blood cell count and absolute value of neutrophils) were significantly higher in the CAS group than in the control group. In addition, 21 species and 142 pathways were enriched in the CAS group, and 10 species and 1 pathway were enriched in the control group. Specifically, Bacteroides eggerthii, Escherichia coli, and Klebsiella pneumoniae were the most abundant species in the CAS group, whereas Parabacteroides unclassified, Prevotella copri, Bacteroides sp 3_1_19, and Haemophilus parainfluenzae were the most abundant species in the control group. Finally, we found that most gut microbes and microbial pathways that were enriched in the CAS group had significant positive correlations with clinical characteristics, whereas the microbes and pathways enriched in healthy controls had significant negative correlations with clinical characteristics excluding high-density lipoprotein cholesterol. In addition, the associations between gut microbes and some microbial pathways (short-chain fatty acid, lipopolysaccharide, and menaquinol biosynthesis) were identified. Our results indicate the existence of a cyclic pathway that elevates the circulating concentrations of trimethylamine-N-oxide in patients with CAS but reduces its concentrations in healthy controls.

The coronavirus disease 2019 (COVID-19) pandemic caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has plunged the world into a major crisis. The disease is characterized by strong infectivity, high morbidity, and high mortality. It is still spreading in some countries. Microbiota and their metabolites affect human physiological health and diseases by participating in host digestion and nutrition, promoting metabolic function, and regulating the immune system. Studies have shown that human microecology is associated with many diseases, including COVID-19. In this research, we first reviewed the microbial characteristics of COVID-19 from the aspects of gut microbiome, lung microbime, and oral microbiome. We found that significant changes take place in both the gut microbiome and airway microbiome in patients with COVID-19 and are characterized by an increase in conditional pathogenic bacteria and a decrease in beneficial bacteria. Then, we summarized the possible microecological mechanisms involved in the progression of COVID-19. Intestinal microecological disorders in individuals may be involved in the occurrence and development of COVID-19 in the host through interaction with ACE2, mitochondria, and the lung-gut axis. In addition, fecal bacteria transplantation (FMT), prebiotics, and probiotics may play a positive role in the treatment of COVID-19 and reduce the fatal consequences of the disease.

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.

Background: Previous observational studies have indicated that an imbalance in gut microbiota may contribute to non-alcoholic fatty liver disease (NAFLD). However, given the inevitable bias and unmeasured confounders in observational studies, the causal relationship between gut microbiota and NAFLD cannot be deduced. Therefore, we employed a two-sample Mendelian randomization (TSMR) study to assess the causality between gut microbiota and NAFLD.Methods: The gut microbiota-related genome-wide association study (GWAS) data of 18,340 individuals were collected from the International MiBioGen consortium. The GWAS summary data for NAFLD from the Anstee cohort (1,483 cases and 17,781 controls) and the FinnGen consortium (894 cases and 217,898 controls) were utilized in the discovery and verification phases, respectively. The inverse variance weighted (IVW) method was used as the principal method in our Mendelian randomization (MR) study, with sensitivity analyses using the MR-Egger, weighted median, simple mode, and weighted mode methods. The MR-Egger intercept test, Cochran’s Q test, and leave-one-out analysis were conducted to identify heterogeneity and pleiotropy. Moreover, a fixed-effect meta-analysis was conducted to verify the robustness of the results.Results: The gene prediction results showed that at the genus level, four gut microbiota were causally associated with NAFLD in the GWAS conducted by Anstee et al. The relative abundance of Intestinimonas (OR: 0.694, 95%CI: 0.533–0.903, p = 0.006, IVW), Lachnoclostridium (OR: 0.420, 95%CI: 0.245–0.719, p = 0.002, IVW), and Senegalimassilia (OR: 0.596, 95%CI: 0.363–0.978, p = 0.041, IVW) was negatively associated with NAFLD. The relative abundance of Ruminococcus1 (OR: 1.852, 95%CI: 1.179–2.908, p = 0.007, IVW) was positively correlated with NAFLD. Among them, the Lachnoclostridium genus was validated in FinnGen GWAS (OR: 0.53, 95%CI: 0.304–0.928, p = 0.026, IVW). The Lachnoclostridium genus was also significantly associated with NAFLD risk in the meta-analyses (OR: 0.470, 95%CI: 0.319–0.692, p = 0.0001, IVW). No heterogeneity or pleiotropy was observed.Conclusion: This study provided new evidence of the relationship between the Lachnoclostridium genus and NAFLD, suggesting that augmentation of the relative abundance of the Lachnoclostridium genus through the oral administration of probiotics or fecal microbiota transplantation could be an effective way to reduce the risk of NAFLD.