Host-bacteria metabolic crosstalk drives S. aureus biofilm
Authors:Kira L. Tomlinson1 and Sebastián A. Riquelme1
doi: 10.15698/mic2021.05.749
Volume 8, pp. 106 to 107, published 19/04/2021.
1 Department of Pediatrics, Columbia University, New York, NY 10032, USA.
Keywords:
Staphylococcus aureus, biofilm, pneumonia, itaconate, immunometabolism.
Corresponding Author(s):
Conflict of interest statement:
Authors declare no conflicts of interest.
Please cite this article as:
Kira L. Tomlinson and Sebastián A. Riquelme (2021). Host-bacteria metabolic crosstalk drives S. aureus biofilm. Microbial Cell 8(5): 106-107. doi: 10.15698/mic2021.05.749
© 2021 Tomlinson and Riquelme. This is an open-access article released under the terms of the Creative Commons Attribution (CC BY) license, which allows the unrestricted use, distribution, and reproduc-tion in any medium, provided the original author and source are acknowledged.
Abstract:
Staphylococcus aureus is a prominent pathogen that can cause intractable lung infections in humans. S. aureus persists in the airway despite inflammation and immune cell recruitment by adapting to host-derived antimicrobial factors. A key component of the immune response to infection are host metabolites that regulate inflammation and bacterial survival. In our recent paper (Tomlinson et al., Nat Commun, doi: 10.1038/s41467-021-21718-y), we demonstrated that S. aureus induces the production of the immunoreglatory metabolite itaconate in airway immune cells by stimulating mitochondrial oxidant stress. Itaconate in turn inhibited S. aureus glycolysis and growth, and promoted carbon flux through bacterial metabolic pathways that support biofilm production. These itaconate-induced metabolic changes were recapitulated in a longitudinal series of clinical isolates from a patient with chronic staphylococcal lung infections, demonstrating a role for host immunometabolism in driving bacterial persistence during long-term staphylococcal lung infections.