| First Author | Eisele NA | Year | 2013 |
| Journal | Cell Host Microbe | Volume | 14 |
| Issue | 2 | Pages | 171-182 |
| PubMed ID | 23954156 | Mgi Jnum | J:315290 |
| Mgi Id | MGI:6830019 | Doi | 10.1016/j.chom.2013.07.010 |
| Citation | Eisele NA, et al. (2013) Salmonella require the fatty acid regulator PPARdelta for the establishment of a metabolic environment essential for long-term persistence. Cell Host Microbe 14(2):171-182 |
| abstractText | 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, PPARdelta, a eukaryotic transcription factor involved in sustaining fatty acid metabolism, is upregulated in Salmonella-infected macrophages. PPARdelta deficiency dramatically inhibits Salmonella replication, which is linked to the metabolic state of macrophages and the level of intracellular glucose available to bacteria. Pharmacological activation of PPARdelta increases glucose availability and enhances bacterial replication in macrophages and mice, while Salmonella fail to persist in Ppardelta null mice. These data suggest that M2 macrophages represent a unique niche for long-term intracellular bacterial survival and link the PPARdelta-regulated metabolic state of the host cell to persistent bacterial infection. |
