The article explores the communication between bacteria and host cells through quorum sensing (QS) systems, focusing on the role of hormones in this interaction. Enterohemorrhagic Escherichia coli (EHEC) O157:H7, responsible for outbreaks of bloody diarrhea, uses a QS system involving the LuxS/AI-2 pathway to sense its presence in the intestine and activate genes essential for colonization. However, the study reveals that an EHEC *luxS* mutant, unable to produce the bacterial autoinducer AI-2, can still respond to a eukaryotic cell signal, specifically the hormone epinephrine (Epi). β- and α-adrenergic antagonists blocked this response, suggesting that AI-2 is not the primary autoinducer involved. Instead, a novel autoinducer, AI-3, produced by the presence of LuxS, was identified as the key signal. AI-3 cross-talks with Epi, and both hormones can activate the transcription of virulence genes and type III secretion in the *luxS* mutant. The study suggests that QS might be a "language" through which bacteria and host cells communicate, potentially mediating interactions between the bacterial QS system and host hormone signaling.The article explores the communication between bacteria and host cells through quorum sensing (QS) systems, focusing on the role of hormones in this interaction. Enterohemorrhagic Escherichia coli (EHEC) O157:H7, responsible for outbreaks of bloody diarrhea, uses a QS system involving the LuxS/AI-2 pathway to sense its presence in the intestine and activate genes essential for colonization. However, the study reveals that an EHEC *luxS* mutant, unable to produce the bacterial autoinducer AI-2, can still respond to a eukaryotic cell signal, specifically the hormone epinephrine (Epi). β- and α-adrenergic antagonists blocked this response, suggesting that AI-2 is not the primary autoinducer involved. Instead, a novel autoinducer, AI-3, produced by the presence of LuxS, was identified as the key signal. AI-3 cross-talks with Epi, and both hormones can activate the transcription of virulence genes and type III secretion in the *luxS* mutant. The study suggests that QS might be a "language" through which bacteria and host cells communicate, potentially mediating interactions between the bacterial QS system and host hormone signaling.