Exploring the role of Pseudomonas aeruginosa surface motility in interspecies interactions with Staphylococcus aureus

The polymicrobial nature of many chronic infections makes their eradication challenging. Particularly, coisolation of Pseudomonas aeruginosa and Staphylococcus aureus from airways of people with cystic fibrosis and chronic wound infections is common and associated with severe clinical outcomes. The complex interplay between these pathogens is not fully understood, highlighting the need for continued research to improve the management of chronic infections. This thesis unveils that P. aeruginosa is attracted to S. aureus, invades into neighboring colonies, and secretes anti-staphylococcal factors into the interior of the colony. Upon inhibition of P. aeruginosa motility, and thus invasion, S. aureus colony architecture changes dramatically, whereby S. aureus is not only protected from P. aeruginosa antagonism, but also responds through physiological alterations that may further hamper treatment. Conversely, S. aureus secreted factors that induced P. aeruginosa directional motility, also upregulated multiple competition pathways that may be detrimental to human cells.

These studies reinforce accumulating evidence that spatial structuring can dictate community resilience and reveal that interspecies chemotaxis and bacterial motility are critical drivers of interspecies competition.