Bacteria use quorum sensing (QS), a high-level signaling process employing autoinducer (AI) molecules, to control virulence, biofilm formation, and population-level behaviors. The process is crucial for both Gram-positive and Gram-negative bacteria, affecting their capacity to thrive in diverse environments. In addition, host-derived stress hormones play important roles in the pathogenicity of bacteria through enhanced growth, virulence, and immune evasion. Catecholamines act as siderophores that assist in the acquisition of iron and increase bacterial resistance. QS in Gram-negative bacteria is mediated by acyl-homoserine lactones that trigger synchronized gene expression at elevated cell density. In contrast, Gram-positive bacteria utilize a peptide-based signaling system for similar regulatory purposes. The disruption of QS by quorum-quenching mechanisms like enzymatic degradation of AI molecules, receptor antagonists, or the inhibition of gene activation are very promising avenues for controlling bacterial infections and antimicrobial resistance. Additionally, bacterial QS systems interact with host endocrine signaling, enabling pathogens to exploit stress-induced hormonal alterations for survival. This cross-kingdom communication underscores the need for targeted interventions, interfering with bacterial signaling without disrupting host–microbe homeostasis. It is critical to comprehend QS-host-derived hormone complex interaction in order to innovate novel anti-microbial strategies, particularly in the healthcare and aquaculture sectors, where bacterial infection poses a critical threat.