The Global Initiative defines COPD for chronic obstructive lung disease as an entirely preventable and treatable disease characterized by sputum production, bacterial colonisation, neutrophilic bronchial airway inflammation and poor health status. The World Health Organization (WHO) estimates that COPD will become the fourth-most common cause of death worldwide, just behind ischemic heart disease, cerebrovascular disease and HIV/AIDS, by 2030. The aim of this study was to determine the main structure feature of sputum potentially pathogenic microorganisms in subjects with COPD during the clinical stable state. We employed a molecular genetics-based investigation of the bacteria community, including DNA isolation, PCR amplification and DGGE profiling. PCR-denaturing gradient gel electrophoresis (DGGE) with universal primers targeting the V3 region of the 16S rRNA gene was employed to characterize the overall COPD patient sputum microbiota composition, and some excised gel bands were cloned for sequencing. Real-time PCR was further utilized to quantitatively analyze the subpopulation of microbiota using group-specific primers targeting Streptococcus pneumoniae, Klebsiella pneumoniae, Pseudomonas aeruginosa. The DGGE profiles of two groups displayed significant differences between COPD and healthy groups (P < 0.05). Real-time PCR revealed significant increases of Streptococcus pneumoniae, Klebsiella pneumoniae and Pseudomonas aeruginosa (P < 0.05) in the COPD group compared with the healthy group. This study revealed strong relationship between alterations of sputum microbiota and COPD. By determining the content of several types of bacteria, we can provide evidence to aid in the diagnosis and treatment of COPD.

Bacterial liver abscess (BLA), accounting for approximately 80% of all liver abscesses, is a severe suppurative infection of the liver. Although gut microbiota dysbiosis has been implicated in BLA pathogenesis, causal evidence remains limited. Here, we integrate Mendelian randomization (MR) and clinical cohort studies to systematically evaluate the causal role of gut microbiota in BLA. Using summary-level genetic data from MiBioGen, GWAS Catalog, and the Pan-UK Biobank, we identified several causal microbial taxa: Coprococcus, Veillonellaceae (including Dialister), and Klebsiella were positively associated with BLA risk, whereas Bacteroides and Bifidobacterium appeared protective. Clinical validation confirmed significant enrichment of Veillonella, Dialister, and Streptococcus in the gut and oral microbiota of BLA patients, contrasting with the predominance of Bacteroides and Bifidobacterium in healthy controls. Klebsiella was the most abundant genus in abscess pus, and gut microbial metabolic profiling revealed marked upregulation of glycolytic pathways in BLA patients. These results indicate that gut dysbiosis exacerbates BLA development through microenvironmental disruption and metabolic reprogramming. Our findings provide mechanistic insights into BLA etiology and suggest microbiota-targeted interventions as promising strategies for prevention and treatment.