Antibacterial contact-dependent proteins secreted by Gram-negative cystic fibrosis respiratory pathogens

• Published in: Trends in microbiology (Regular ed.) 2022-10, Vol.30 (10), p.986-996
• Main Authors: Crisan, Cristian V., Goldberg, Joanna B.
• Format: Article
• Language: English
• Subjects: bacterial pathogens; cystic fibrosis; secretion systems; toxins
• ISSN: 0966-842X; 1878-4380
• DOI: 10.1016/j.tim.2022.03.009

Cystic fibrosis (CF) is a genetic disease that affects almost 100 000 people worldwide. CF patients suffer from chronic bacterial airway infections that are often polymicrobial and are the leading cause of mortality. Interactions between pathogens modulate expression of genes responsible for virulence and antibiotic resistance. One of the ways bacteria can interact is through contact-dependent systems, which secrete antibacterial proteins (effectors) that confer advantages to cells that harbor them. Here, we highlight recent work that describes effectors used by Gram-negative CF pathogens to eliminate competitor bacteria. Understanding the mechanisms of secreted effectors may lead to novel insights into the ecology of bacteria that colonize respiratory tracts and could also pave the way for the design of new therapeutics. Cystic fibrosis (CF) is an inherited disease that negatively impacts the lives of almost 100 000 people worldwide; chronic polymicrobial respiratory infections are critical to patient outcome.Opportunistic Gram-negative bacterial pathogens, such as Pseudomonas aeruginosa, members of the Burkholderia cepacia complex, and Stenotrophomonas maltophilia, can be coisolated from the lungs of CF patients.Contact-dependent inhibition systems may allow CF pathogens to eliminate bacteria from the same or closely related species.P. aeruginosa and Burkholderia species can deliver antibacterial proteins via a Type VI secretion system to alter the target bacterial cells’ metabolism and degrade the cell envelope.S. maltophilia can use a Type IV secretion system to translocate antibacterial proteins that contribute to the pathogen’s competitive fitness.