Host-bacteria metabolic crosstalk drives S. aureus biofilm

is a prominent pathogen that can cause intractable lung infections in humans. 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 , Nat Commun, doi: 10.1038/s41467-021-21718-y), we demonstrated that induces the production of the immunoregulatory metabolite itaconate in airway immune cells by stimulating mitochondrial oxidant stress. Itaconate in turn inhibited 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.