Persistent infections force the host to develop compensatory mechanisms to prevent organ damage, which are collectively called disease tolerance. Here authors show in a Pseudomonas aeruginosa murine infection model that an alginate-itaconate metabolic interplay, creating metabolic synchrony between the host and the pathogen plays a role in mitigating harmful inflammation.
- Ying-Tsun Chen
- Gaurav Kumar Lohia
- Sebastián A. Riquelme
