Qingyang Wu

Background: About 20% of patients with coronary artery disease (CAD) experience adverse events within five years of undergoing percutaneous coronary intervention (PCI) for acute myocardial infarction. In these patients, the impact of metformin on long-term prognosis remains uncertain. Methods: This study enrolled 22 metformin (Met)-CAD patients with diabetes mellitus (DM) who had been administered metformin for at least six months before PCI, 14 non-Met CAD-DM patients with DM who had never taken metformin or had stopped taking metformin for a year before PCI, and 22 matched healthy controls. A 5-year follow-up was conducted to collect clinical prognosis data. Fecal 16S rRNA sequencing and serum untargeted metabolomics analyses were performed. BugBase was utilized to analyze the possible functional changes in the gut microbiome. Multi-omics analysis was conducted using Spearman’s correlation to explore the interactions between metformin, gut microbiome, serum metabolites, and clinical prognosis. Results: Metformin significantly lowered the 5-year major adverse cardiac events (MACEs) in Met CAD-DM patients. We found a higher abundance of Bacteroides coprocola, Bacteroides massiliensis, Phascolarctobacterium succinatutens, and Eubacterium coprostanoligenes in the Met CAD-DM patients, as well as an increase in hydroxy-alpha-sanshool (HAS) and decenoylcarnitine and a decrease in tridec-10-enoic acid, Z-vad-fmk (benzyloxycarbonyl–Val–Ala–Asp (OMe)–fluoromethylketone), 3,9-dimethyluric acid in blood serum. Multi-omics analysis revealed that alterations in the gut microbiome and serum metabolites are significantly associated with the 5-year prognosis of CAD-DM. Conclusions: Metformin significantly improved the 5-year prognosis of CAD patients following PCI. Metformin tended to have more positive effects on the commensal flora and metabolic profiles, which may explain its beneficial effects on cardiovascular health. This study revealed the potential associations between metformin and the gut microbiome, an associated alteration in serum metabolome, and the impact on the host immune system and metabolic pathways.

Background: Pemphigus is a group of potentially life-threatening autoimmune bullous diseases induced by pathogenic autoantibodies binding to the surface of epidermal cells. The role of the gut microbiota (GM) has been described in various autoimmune diseases. However, the impact of the GM on pemphigus is less understood. This study aimed to investigate whether there was alterations in the composition and function of the GM in pemphigus patients compared to healthy controls (HCs). Methods: Fecal samples were collected from 20 patients with active pemphigus (AP), 11 patients with remission pemphigus (PR), and 47 HCs. To sequence the fecal samples, 16S rRNA was applied, and bioinformatic analyses were performed. Results: We found differences in the abundance of certain bacterial taxa among the three groups. At the family level, the abundance of Prevotellaceae and Coriobacteriaceae positively correlated with pathogenic autoantibodies. At the genus level, the abundance of Klebsiella, Akkermansia, Bifidobacterium, Collinsella, Gemmiger, and Prevotella positively correlated with pathogenic autoantibodies. Meanwhile, the abundance of Veillonella and Clostridium_XlVa negatively correlated with pathogenic autoantibodies. A BugBase analysis revealed that the sum of potentially pathogenic bacteria was elevated in the AP group in comparison to the PR group. Additionally, the proportion of Gram-negative bacteria in the PR group was statistically significantly lower in comparison to the HC group. Conclusion: The differences in GM composition among the three groups, and the correlation between certain bacterial taxa and pathogenic autoantibodies of pemphigus, support a linkage between the GM and pemphigus.

With the explosion research on the gut microbiome in the recent years, much insight has been accumulated in comprehending the crosstalk between the gut microbiota community and host health. Acute pancreatitis (AP) is one of the gastrointestinal diseases associated with significant morbidity and subsequent mortality. Studies have elucidated that gut microbiota are engaged in the pathological process of AP. Herein, we summarize the major roles of the gut microbiome in the development of AP. We then portray the association between dysbiosis of the gut microbiota and the severity of AP. Finally, we illustrate the promises and challenges that arise when seeking to incorporate the microbiome in acute pancreatitis treatment.

Bullous pemphigoid (BP) is a severe autoimmune blistering disease affecting patients' quality of life. Gut microbiota (GM) dysbiosis have been investigated to be associated with multiple autoimmune diseases. However, the relationship between GM and BP onset and remission remains to be established by a systematic study. We conducted a study that enrolled 24 patients with BP onset (BP group), 24 patients under remission stage (BP‐R group) and 24 healthy controls (HC group). We applied 16S rRNA sequencing on faecal samples and revealed a separation of the microbiota structure. At the family level, Lachnospiraceae, Prevotellaceae and Veillonellaceae were more abundant in the HC and BP‐R groups, while Bacteroidaceae, Ruminococcaceae and Enterobacteriaceae were more abundant in the BP group. Bugbase analysis revealed the potentially pathogenic bacteria had an increasing trend in the BP group compared with the HC group and this variation vanished in the BP‐R group. At the amplicon sequence variants (ASV) level, Bacteroides ovatus (ASV40) and Veillonella dispar (ASV140) significantly decreased, while Prevotella copri (ASV54) increased in the BP group compared to the HC and BP‐R groups. The HC group and BP‐R group shared similar abundance. Furthermore, by correlation analysis, we investigated key ASVs correlated with clinical parameters and found some discriminate biomarkers between the BP and BP‐R groups. Our study established a dynamic GM profile in BP patients under different disease activity, providing a new direction to understand the role of GM in BP pathogenesis and therapeutic effects.