Alterations in gut microbiota and host transcriptome of patients with coronary artery disease Original paper

What was studied?

This original study investigated how alterations in the gut microbiota interact with host blood transcriptomic activity in coronary artery disease (CAD), forming an integrated microbiome–transcriptome signature of disease. The researchers profiled fecal 16S rRNA sequences and peripheral blood mononuclear cell (PBMC) gene expression to identify microbial and host gene biomarkers linked to CAD. The central aim was to determine whether gut microbes—particularly short-chain fatty acid (SCFA) producers—and their microbial functions correlate with CAD-associated transcriptomic pathways and clinical cardiac biomarkers, potentially yielding microbiome signatures useful for early detection.

Who was studied?

The study examined 31 CAD patients and 21 matched healthy controls recruited from a cardiology center, all with coronary angiography to confirm disease severity. CAD patients showed ≥70% stenosis in at least one major coronary artery, whereas controls had ≤20% stenosis. Fecal samples were collected from all 52 participants, and blood transcriptomic samples were available for 50 individuals. Baseline demographic and clinical characteristics, including age, medications, and comorbidities, were comparable between groups, allowing microbial and transcriptomic differences to be attributed more directly to CAD status.

Most important findings

Key microbiome-related findings include significant shifts in gut microbial composition despite unchanged alpha diversity. Eighteen genera showed differential abundance: SCFA-producing genera Blautia, Eubacterium, Fusicatenibacter, and Monoglobus were depleted in CAD, while Sutterella, Collinsella, Negativibacillus, Colidextribacter, Faecalitalea, and others were enriched. Beta-diversity analyses on page 4 visually confirmed a distinct community structure separation between CAD and controls. A Random Forest model identified 20 bacterial biomarkers with good discriminative power (AUC 0.81), and combining microbial and gene markers improved accuracy to AUC 0.92. Functionally, CAD microbiomes showed downregulation of beta-lactam and CAMP resistance pathways and upregulation of nitrogen and methane metabolism and alkaloid biosynthesis (page 6). Several enriched genera correlated positively with heart-related clinical markers—including troponin I, BNP, and creatine kinase—linking dysbiosis to cardiac injury profiles. Transcriptomic analysis revealed 409 upregulated and 762 downregulated genes in CAD, with depletion of interferon-related pathways and enrichment of inflammatory signaling (page 7). Integration highlighted strong correlations between Fusicatenibacter and CAD-risk genes such as GBP2, MLKL, and GPR65—genes previously implicated in atherosclerosis, necroptosis, and immune signaling. Microbial depletion patterns closely tracked reduced interferon signaling, suggesting functional host–microbe synergy in CAD.

Key implications

These results suggest that CAD is accompanied by depletion of beneficial SCFA-producing gut microbes and parallel suppression of host interferon pathways, creating a microbiome–immune landscape that favors inflammation and cardiovascular dysfunction. The microbial genera Blautia, Eubacterium, Fusicatenibacter, and Monoglobus emerge as central to this pattern, making them strong candidates for microbiome signatures in CAD risk stratification. Coupled microbial and gene biomarkers offer enhanced diagnostic capability, reinforcing the potential for integrated multi-omic tools in early CAD detection and mechanistic insight.

Citation

Chen L, Mou X, Li J, et al. Alterations in gut microbiota and host transcriptome of patients with coronary artery disease. BMC Microbiology. 2023;23:320. doi:10.1186/s12866-023-03071-w