The Gut-Spine Axis in Lumbar Intervertebral Disc Degeneration: Microbial and Inflammatory Signatures

Intervertebral disc degeneration (IDD) is commonly found in patients with chronic low back pain. Traditionally viewed as a biomechanical failure, emerging evidence implicates systemic inflammation in IDD pathogenesis. The proposed "gut-spine axis," in which gut dysbiosis may promote inflammation and, potentially, disc colonization, represents a paradigm shift. To bridge gaps in human data, we present the first multi-compartment (gut-blood-disc) study profiling paired microbiomes alongside systemic inflammatory biomarkers.

To investigate the role of the gut-spine axis in intervertebral disc degeneration (IDD) by characterizing gut microbiome dysbiosis, its association with systemic inflammation, and the presence of distinct microbial signatures in degenerated disc tissue.

Prospective clinical case-control study conducted at a tertiary care center.

Twenty adult patients (aged 18-65 years) undergoing surgical discectomy for symptomatic lumbar IDD (Pfirrmann grade ≥3) and twenty age-matched healthy controls without low back pain or radiographic evidence of IDD.

Primary outcomes included gut and disc microbial diversity (alpha diversity indices: Shannon, Simpson, observed genera; beta diversity: Bray Curtis dissimilarity), genus level relative abundance of key microbial organisms, and systemic inflammatory status assessed using the neutrophil-to-lymphocyte ratio (NLR). Secondary outcomes included associations between microbial organisms and systemic inflammation.

We prospectively analyzed patients undergoing lumbar IDD surgery alongside matched healthy controls. Paired fecal and surgically excised disc samples underwent 16S rRNA sequencing. Systemic inflammation was quantified via the peripheral neutrophil-to-lymphocyte ratio (NLR). We evaluated alpha- and beta-diversity and employed linear regression to assess functional associations between microbial abundance and NLR RESULTS: Patients with symptomatic IDD exhibited significant gut dysbiosis, including elevated Streptococcus and a 7-fold enrichment of Collinsella (10% in IDD vs. 1.5% in controls). Fecal Acinetobacter positively correlated with systemic inflammation (NLR; R²=0.326, p=0.009), whereas beneficial Dorea negatively correlated (R²=0.230, p=0.032). Locally, degenerated discs harbored a unique, low-diversity microbiome (Simpson index p=0.038) dominated by the facultative anaerobes Acinetobacter and Stenotrophomonas (32% relative abundance vs. <1% in gut). Beta-diversity confirmed disc and gut communities are statistically distinct (PERMANOVA R²=0.451, p=0.001), a pattern more consistent with compartment-specific microbial communities than with surgical contamination.

This study provides preliminary evidence for a potential functional gut-spine axis in symptomatic lumbar IDD. We show that IDD is associated with a pro-inflammatory gut dysbiosis that correlates with systemic inflammation. Furthermore, the identification of a unique, pathobiont-enriched microbiome within the degenerated disc challenges the view of IDD as a sterile condition. These findings suggest that IDD may have a systemic component, and point to microbiome-targeted diagnostics and therapeutics as potential avenues for future intervention.