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Published on: May 6, 2013
Salmonella-liberated dietary L-arabinose promotes expansion in superspreaders
Sarah J Ruddle1, Liliana M Massis1, Alyssa C Cutter1
1Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Abstract:
The molecular understanding of host-pathogen interactions in the gastrointestinal (GI) tract of superspreader hosts is incomplete. In a mouse model of chronic, asymptomatic Salmonella enterica serovar Typhimurium (S. Tm) infection, we performed untargeted metabolomics on the feces of mice and found that superspreader hosts possess distinct metabolic signatures compared with non-superspreaders, including differential levels of L-arabinose. RNA-seq on S. Tm from superspreader fecal samples showed increased expression of the L-arabinose catabolism pathway in vivo. By combining bacterial genetics and diet manipulation, we demonstrate that diet-derived L-arabinose provides S. Tm a competitive advantage in the GI tract, and expansion of S. Tm in the GI tract requires an alpha-N-arabinofuranosidase that liberates L-arabinose from dietary polysaccharides. Ultimately, our work shows that pathogen-liberated L-arabinose from the diet provides a competitive advantage to S. Tm in vivo. These findings propose L-arabinose as a critical driver of S. Tm expansion in the GI tracts of superspreader hosts.
Insights
Dietary L-arabinose fuels Salmonella Typhimurium expansion in superspreader hosts. This sugar provides a competitive edge, requiring specific enzymes for its release from food, highlighting a key factor in pathogen growth.
Area of Science:
- Microbiology
- Host-Pathogen Interactions
- Gastrointestinal Tract Microbiome
Background:
- Host-pathogen interactions in the gastrointestinal (GI) tract, particularly in superspreader hosts, remain incompletely understood.
- Salmonella enterica serovar Typhimurium (S. Tm) infections can be asymptomatic yet lead to superspreading events.
Purpose of the Study:
- To investigate the metabolic differences in the GI tract of S. Tm superspreader mice.
- To elucidate the role of diet-derived metabolites in S. Tm pathogenesis and expansion.
Main Methods:
- Untargeted fecal metabolomics in a mouse model of chronic S. Tm infection.
- RNA sequencing (RNA-seq) of S. Tm from superspreader and non-superspreader mice.
- Bacterial genetics and dietary manipulation experiments.
Main Results:
- Superspreader hosts exhibit distinct fecal metabolic signatures, notably altered L-arabinose levels.
- Increased expression of the L-arabinose catabolism pathway in S. Tm within superspreader hosts.
- Diet-derived L-arabinose confers a competitive advantage to S. Tm, with alpha-N-arabinofuranosidase essential for its liberation and pathogen expansion.
Conclusions:
- Dietary L-arabinose is a critical factor driving S. Tm expansion in the GI tracts of superspreader hosts.
- The liberation of L-arabinose from dietary polysaccharides by S. Tm is essential for its in vivo proliferation.
- Targeting L-arabinose metabolism presents a potential strategy to control S. Tm infections in superspreader individuals.
