Alteration of the Brains Microbiome and Neuroinflammation Associated with Ventricular Catheters

Background and Objectives: Proximal catheter obstruction is the leading cause of ventriculoperitoneal shunt failure, yet the biological triggers of peri-catheter inflammation and tissue ingrowth remain poorly defined. Evidence of bacterial ribosomal RNA in human brain tissue suggests that low-biomass microbial exposure may influence the inflammatory microenvironment surrounding implants. This study examined if microbial signal is detectable in unaltered brain tissue and if catheter implantation produces microbial shifts relevant to shunt dysfunction. Methods: Twenty-nine female mice were assigned to unaltered control (UC), trauma control (TC), plain silicone catheter (PSC), or antibiotic-impregnated catheter (AIC) groups. Brain and cecum tissues were harvested at postoperative days 7 and 28 for 16S rRNA sequencing. Microbial composition and predicted functional pathways were analyzed. A separate cohort underwent longitudinal MRI to assess edema, glial scar formation, and macrophage-associated susceptibility signal. Results: Low-level microbial signal was detected in unaltered brain tissue. Catheter implantation induced material-dependent shifts in brain-associated microbial composition. PSC was associated with enrichment of pro-inflammatory taxa, whereas AIC favored immune-regulatory taxa. Predicted short-chain fatty acid biosynthesis was highest in AIC and lowest in PSC, while predicted lipopolysaccharide biosynthesis trended higher in PSC. MRI showed similar edema resolution but higher macrophage-associated susceptibility signal in PSC animals. Conclusion: Intracranial catheter implantation produces material-dependent shifts in low-biomass brain-associated microbial signal that parallel differential neuroimmune activation. These findings suggest catheter material may shape a biologically relevant peri-catheter niche with implications for chronic gliosis and proximal shunt obstruction.