Boron as a Molecular Architect of Host–Microbiome Symbiosis: Implications for Dysbiosis and Aging-Related Pathologies

Boron (B) is increasingly recognized as more than a trace dietary element, emerging as a context-dependent organizer of molecular interactions at the host–microbiome interface. B exhibits reversible covalent chemistry driven by Lewis’ acidity and selective affinity for cis-diol-rich biomolecules, enabling dynamic complexation with polyols, glycans, and phenolic ligands that dominate the intestinal mucus environment and shape microbial ecology. We synthesize evidence supporting an architecture-based framework in which B modulates biological function by conditioning the physicochemical context of microbial communication rather than acting as a single-pathway effector. Central to this model is spatial bioavailability, distinguishing plasma-accessible boron from microbiota-accessible boron (MAB), species that persist in the lumen and mucus layer long enough to influence interface-level processes. We propose that insufficient or altered MAB availability may contribute to dysbiosis (DYS) by destabilizing quorum-associated coordination, signal persistence, and mucosal microstructure, thereby promoting barrier dysfunction and inflammaging. Particular attention is given to B-mediated symbiotaxis, a hypothesis-driven concept describing how B-containing molecular assemblies may bias microbial communities toward cooperative, barrier-supportive configurations and reduce ecological volatility. We identify key knowledge gaps and experimental priorities (speciation-aware measurements, signal-centric readouts) necessary to determine when, where, and how B-mediated molecular architecture may counteract DYS and support healthspan.