Catecholamines modulate pathogen-probiotic-host interactions: insights from Pseudomonas aeruginosa and Pediococcus pentosaceus
TL;DR
It is demonstrated that catecholamines can modulate competitive interactions between commensal and pathogenic bacteria, suggesting that host neuroendocrine signals may contribute to shaping microbial community dynamics, regulating host–microbiota homeostasis, and influencing infection processes.
Abstract
Stress-related catecholamine hormones, including epinephrine (Epi), norepinephrine (NE), and dopamine (Dopa), are increasingly recognized as modulators of bacterial physiology. However, the human microbiota represents a highly interconnected network of commensal and pathogenic species that continuously respond to host-derived and environmental cues, and how these signals influence interspecies interactions within microbial communities remains poorly understood. Here, we investigated the impact of catecholamines on the interaction between the pathogen Pseudomonas aeruginosa H103 and the probiotic Pediococcus pentosaceus MZF16. Catecholamine exposure increased the total biomass of dual-species biofilms while maintaining the predominance of MZF16. These hormones also modified bacterial co-aggregation and adhesion to abiotic surfaces and enhanced the anti-adhesion activity of MZF16 against P. aeruginosa H103 in human intestinal epithelial cells. Moreover, NE modulated the virulence of H103 in the presence of the probiotic strain, with distinct effects observed in human cells and in the Galleria mellonella infection model. Together, these findings demonstrate that catecholamines can modulate competitive interactions between commensal and pathogenic bacteria, suggesting that host neuroendocrine signals may contribute to shaping microbial community dynamics, regulating host–microbiota homeostasis, and influencing infection processes.