Beyond bacterial communication: host factors that modulate quorum sensing and virulence in human pathogens

Quorum sensing (QS) coordinates collective bacterial behavior, but during infection, its activity is also shaped by host biology. This review examines how host-derived factors modulate QS-linked virulence in enteric pathogens, Pseudomonas aeruginosa and Staphylococcus aureus. Across these systems, host control operates through three recurring modes: activation or signal mimicry, enzymatic signal degradation, and extracellular sequestration or receptor-level interference. Catecholamines and related metabolites can feed into bacterial sensory pathways and promote virulence signaling; PONs (paraoxonases) and other host enzymes can degrade autoinducers; and lipoproteins, immune mediators, and epithelial surveillance systems can intercept or reinterpret quorum signals. Together, these data support the view that the host is an active signal-processing environment that reshapes colonization, persistence, and tissue damage, and they point to host-inspired anti-virulence strategies that target signaling rather than viability.