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Staphylococcal secreted cytotoxins are competition sensing signals for Pseudomonas aeruginosa
Preprint   Open access

Staphylococcal secreted cytotoxins are competition sensing signals for Pseudomonas aeruginosa

Grace Wang, Elizabeth Warren, Allison Haas, Andrea Sánchez Peña, Megan Kiedrowski, Brett Lomenick, Tsui-Fen Chou, Jennifer Bomberger, David Tirrell and Dominique Limoli
bioRxiv
Cold Spring Harbor Laboratory Press
01/29/2023
DOI: 10.1101/2023.01.29.526047
PMCID: PMC9900984
PMID: 36747623
url
https://doi.org/10.1101/2023.01.29.526047View
Preprint (Author's original)This preprint has not been evaluated by subject experts through peer review. Preprints may undergo extensive changes and/or become peer-reviewed journal articles. Open Access

Abstract

Coinfection with two notorious opportunistic pathogens, the Gram-negative Pseudomonas aeruginosa and Gram-positive Staphylococcus 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 between P. aeruginosa and S. aureus. We discovered that P. aeruginosa senses S. aureus secreted peptides and, counterintuitively, moves towards these toxins. P. aeruginosa tolerates 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 full P. aeruginosa competition with S. 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. Competing Interest Statement The authors have declared no competing interest.
Antagonism Competition Cytotoxins Molecular modelling Opportunist infection Pseudomonas aeruginosa Staphylococcus aureus

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