ArticleCell host & microbe2013
Salmonella require the fatty acid regulator PPARδ for the establishment of a metabolic environment essential for long-term persistence.
Article in Cell host & microbe, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 137 papers.
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Who cites it
137 citing papers in PubMed, 218 citations in OpenAlex.
- Host-microbiota-pathogen interactions drive Salmonella enterica serovar Typhimurium pathogenesis.Nature reviews. Microbiology · 2026Review
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- Provision of preferred nutrients to macrophages promotes Salmonella intracellular replication without relying on Type III secretion systems.PLoS pathogens · 2026Article
- SPIC-dependent erythrophagocytic macrophages drive granuloma formation and pathogen persistence during intracellular bacterial infection.bioRxiv : the preprint server for biology · 2026Article
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- LuxS/AI-2 regulates phoP/phoQ by a non-canonical mechanism to enhance acid stress survival in Salmonella Typhimurium.PLoS pathogens · 2026Article
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- Glycolytic reprogramming and immune responses in macrophages: a crosstalk driven by bacterial infection.Frontiers in immunology · 2026Review
- Restriction of mitochondrial oxidation of glutamine or fatty acids enhances intracellular growth ofVirulence · 2025Article
- Blood-borne immune cells carry low biomass DNA remnants of microbes in patients with colorectal cancer or inflammatory bowel disease.Gut microbes · 2025Article
- Pp6-Pfkfb1 axis modulates intracellular bacterial proliferation by orchestrating host-pathogen metabolic crosstalk.PLoS pathogens · 2025Article
- Eosinophils enhance granuloma-mediated control of persistent Salmonella infection in mice.Nature microbiology · 2025Article
- tRF-His-GTG-1 promotes Salmonella survival through modulation of lipid metabolism and immune signaling.Cell communication and signaling : CCS · 2025Article
- NarL gene modulates the host lipid metabolism for survival of Salmonella Typhimurium in murine macrophages.Molecular biology reports · 2025Article
- Loss of NR2F6 Protects from Salmonella Typhimurium Infection.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Phase-Specific Dynamics in Gene Expression of Salmonella Typhimurium During Acanthamoeba castellanii Infection.Current microbiology · 2025Article
- Antibiotic-recalcitrant Salmonella during infection.Nature reviews. Microbiology · 2025Review
- RBM43 controls PGC1α translation and a PGC1α-STING signaling axis.Cell metabolism · 2025Article
- Article
77 more citing papers are in PubMed but not listed here.
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9 authors at 2 institutions in 1 country.
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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 available to bacteria. Pharmacological activation of PPARδ increases glucose availability and enhances bacterial replication in macrophages and mice, while Salmonella fail to persist in Pparδ null mice. These data suggest that M2 macrophages represent a unique niche for long-term intracellular bacterial survival and link the PPARδ-regulated metabolic state of the host cell to persistent bacterial infection.
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