Results
Alpha diversity of gut microbiota was significantly reduced in brucellar spondylitis patients compared to healthy controls, with increased microbial community homogeneity.
- Study recruited 20 BLS patients and 20 healthy donors
- Multi-omics analysis including metagenomics, untargeted metabolomics, and targeted short-chain fatty acids (SCFAs) analysis were used
- Beta diversity analysis revealed significant differences in microbial community structure between groups
- Disease progression was associated with an overall imbalance in gut microbiota and deterioration of its specific structural composition
Results
At the phylum level, abundances of Actinomycetota, unclassified_d_Viruses, and Fusobacteriota were significantly increased in BLS patients, while Bacillota and Pseudomonadota were significantly decreased.
- Comparison was made between 20 BLS patients and 20 healthy controls
- Metagenomics was the analytical method used for microbial community profiling
- Both increases and decreases in specific phyla were observed, indicating bidirectional dysbiosis
- These phylum-level changes reflected an overall restructuring of the gut microbial ecosystem in BLS
Results
At the genus level, Enterococcus abundance was significantly increased in BLS patients, while multiple butyrate-producing genera were significantly decreased.
- Genera significantly decreased included Blautia, Faecalibacterium, Ruminococcus, Agathobacter, Roseburia, Clostridium, Eubacterium, Alistipes, and Anaerobutyricum
- At the species level, Enterococcus sp and Enterococcus faecium were increased
- Decreased species included Blautia sp, Ruminococcus sp, Faecalibacterium sp, Faecalibacterium prausnitzii, Agathobacter rectalis, Eubacterium sp, Agathobacter sp, and Roseburia sp
- Loss of butyrate-producing symbionts was proposed to create ecological niches for facultatively anaerobic Enterococcus
Results
Intestinal levels of short-chain fatty acids including butyrate, isobutyrate, valerate, and 4-methylvalerate were reduced in BLS patients.
- Targeted SCFAs analysis was used to measure intestinal content metabolite levels
- Functional KEGG profiling revealed that key KOs involved in butyrate synthesis (e.g., K00074, K00172, K01640) and transport were globally downregulated in the patient group
- SCFAs deficiency was associated with mucosal barrier disruption in BLS
- The reduction in butyrate-producing bacteria was mechanistically linked to the observed SCFAs deficiency
Results
Untargeted metabolomics revealed enrichment of metabolites in the histidine metabolic pathway, and histidine decarboxylase KOs were significantly enriched in BLS patients.
- Histidine decarboxylase KOs identified as enriched included K01693, K11755, and K19787
- These KOs convert histidine to pro-inflammatory histamine
- Plasma levels of histamine and histidine decarboxylase were measured by ELISA to clarify the role of the differential histidine metabolic pathway
- Enterococcus was proposed to exacerbate local inflammation via proteolytic fermentation and histamine production
Results
BLS patients showed an altered inflammatory cytokine profile, with decreased IL-10 and increased IL-1β, IL-6, IL-17A, and TNF-α compared to healthy controls.
- Plasma cytokine levels were measured by ELISA
- Anti-inflammatory cytokine IL-10 was decreased in BLS patients
- Pro-inflammatory cytokines IL-1β, IL-6, IL-17A, and TNF-α were all increased in BLS patients
- LPS levels were also elevated in BLS patients, suggesting disruption of intestinal integrity and permeability
Results
Plasma LPS levels were significantly elevated in BLS patients, indicating disruption of intestinal integrity and increased intestinal permeability.
- LPS levels were measured by ELISA in plasma samples
- Elevated LPS was interpreted as evidence of mucosal barrier disruption
- Correlation analysis indicated a close relationship between gut microbiota composition and inflammatory indicators including LPS
- SCFAs deficiency and mucosal barrier disruption were proposed as mechanisms linking gut dysbiosis to elevated systemic LPS
Results
Correlation analysis demonstrated a close relationship between gut microbiota composition and inflammatory indicators in BLS patients.
- Correlation analysis was performed between gut microbiota metrics and inflammatory indicators
- The overactivated inflammatory cytokine network was proposed to mediate bone destruction and intervertebral disc damage
- A bidirectional interaction between gut microbiota dysbiosis and inflammatory cytokine networks through the 'gut-spine axis' was suggested
- The findings collectively support the role of intestinal microecological dysbiosis in BLS pathogenesis