ArticlePLoS biology2024
Salmonella Typhimurium exploits host polyamines for assembly of the type 3 secretion machinery.
Article in PLoS biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- The alternative polyadenylation factor CFIm25 orchestrates macrophage antibacterial activity againstInfection and immunity · 2026Article
- Spermine suppressesmBio · 2026Article
- Article
- Amino acid decarboxylation preservesmBio · 2026Article
- Feeding the invaders: how metabolic imbalance shapes infection and biofilm development.FEMS microbiology reviews · 2026Review
- Infection strategies ofGut microbes reports · 2026Review
- 3'UTR-derived small RNA couples acid resistance to metabolic reprogramming of Salmonella within macrophages.Nucleic acids research · 2025Article
- Article
- Defence Warriors: Exploring the crosstalk between polyamines and oxidative stress during microbial pathogenesis.Redox biology · 2025Review
- Outer membrane barrier impairment byMicrobiology (Reading, England) · 2024Article
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Authors and funding
11 authors.
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Abstract
Bacterial pathogens utilize the factors of their hosts to infect them, but which factors they exploit remain poorly defined. Here, we show that a pathogenic Salmonella enterica serovar Typhimurium (STm) exploits host polyamines for the functional expression of virulence factors. An STm mutant strain lacking principal genes required for polyamine synthesis and transport exhibited impaired infectivity in mice. A polyamine uptake-impaired strain of STm was unable to inject effectors of the type 3 secretion system into host cells due to a failure of needle assembly. STm infection stimulated host polyamine production by increasing arginase expression. The decline in polyamine levels caused by difluoromethylornithine, which inhibits host polyamine production, attenuated STm colonization, whereas polyamine supplementation augmented STm pathogenesis. Our work reveals that host polyamines are a key factor promoting STm infection, and therefore a promising therapeutic target for bacterial infection.
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