Abstract The long-standing view of sterile internal tissues has been challenged by accumulating evidence that microbial material, and under specific conditions, viable bacteria may translocate from the gut and oral cavity into metabolic and cardiovascular tissues. This review synthesizes current knowledge on the mechanisms underlying bacterial translocation and its implications for cardiometabolic disease, complemented by original experimental data. Dysbiosis and epithelial barrier disruption facilitate the passage of microbial components and, in some settings, culturable bacteria across mucosal surfaces, triggering local and systemic inflammation. In our murine models, high-fat feeding markedly increased the recovery of culturable bacteria from visceral adipose tissue and spleen, with tissue-specific bacterial signatures enriched in pro-inflammatory taxa. GFP-labelled E. coli translocated more abundantly under metabolic stress, while CD14 deficiency significantly reduced dissemination, highlighting the role of LPS–CD14 signaling. Clinical studies consistently report bacterial DNA and, in some cases, viable bacteria in adipose tissue, liver, atherosclerotic plaques, and heart valves, correlating with immune cell infiltration, cytokine production, and disease severity. However, because internal organs are low-biomass environments, interpretation requires stringent contamination controls and orthogonal evidence of viability and localization. Together, these findings support bacterial translocation as a plausible contributor to chronic low-grade inflammation, insulin resistance, and cardiometabolic pathology. Targeting microbial translocation through barrier reinforcement, microbiota modulation, and metabolite inhibition may offer novel preventive and therapeutic strategies that warrant careful validation.
Minty et al. (2026) studied this question.