Salmonella require the fatty acid regulator PPARδ for the establishment of a metabolic environment essential for long-term persistence.

ABSTRACT: Host-adapted Salmonella strains are responsible for a number of disease manifestations in mammals, including an asymptomatic chronic infection in which bacteria survive within macrophages located in systemic sites. However, the host cell physiology and metabolic requirements supporting bacterial persistence are poorly understood. In a mouse model of long-term infection, we found that S. typhimurium preferentially associates with anti-inflammatory/M2 macrophages at later stages of infection. Further, PPARδ, a eukaryotic transcription factor involved in sustaining fatty acid metabolism, is upregulated in Salmonella-infected macrophages. PPARδ deficiency dramatically inhibits Salmonella replication, which is linked to the metabolic state of macrophages and the level of intracellular glucose a

SUBMITTER: Eisele NA 

PROVIDER: S-EPMC3785333 | biostudies-literature | 2013 Aug

REPOSITORIES: biostudies-literature