Coinfection with two notorious opportunistic pathogens, the Gram-negativePseudomonas aeruginosaand Gram-positiveStaphylococcus aureus, dominates chronic pulmonary infections. While coinfection is associated with poor patient outcomes, the interspecies interactions responsible for such decline remain unknown. Here, we dissected molecular mechanisms of interspecies sensing betweenP. aeruginosaandS. aureus. We discovered thatP. aeruginosasensesS. aureussecreted peptides and, counterintuitively, moves towards these toxins.P. aeruginosatolerates such a strategy through competition sensing, whereby it preempts imminent danger/competition by arming cells with type six secretion (T6S) and iron acquisition systems. Intriguingly, while T6S is predominantly described as weaponry targeting Gram-negative and eukaryotic cells, we find that T6S is essential for fullP. aeruginosacompetition withS. aureus, a previously undescribed role for T6S. Importantly, competition sensing was activated during coinfection of bronchial epithelia, including T6S islands targeting human cells. This study reveals critical insight into both interspecies competition and how antagonism may cause collateral damage to the host environment.

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