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Host-mediated sugar oxidation promotes post-antibiotic pathogen expansion.
Nature
|June 17, 2016
Summary
Antibiotic use can lead to Salmonella expansion in the gut. This study reveals that host-driven oxidation of sugars like galactose and glucose fuels this post-antibiotic pathogen growth.
Area of Science:
- Microbiology
- Gut Microbiome Research
- Infectious Disease Mechanisms
Background:
- Gut microbiota alterations are linked to human diseases, but mechanisms remain unclear.
- Antibiotic use, particularly streptomycin, disrupts gut microbial balance and promotes Salmonella enterica serovar expansion.
- Previous studies show streptomycin treatment in mice leads to Salmonella expansion, but the precise mechanisms are not fully understood.
Purpose of the Study:
- To elucidate the mechanisms by which streptomycin treatment drives the expansion of Salmonella enterica serovar Typhimurium (S. Typhimurium) in the murine gut.
- To identify host-derived factors that promote pathogen growth after antibiotic perturbation.
- To investigate the role of carbohydrate oxidation products in post-antibiotic S. Typhimurium expansion.
Main Methods:
- Administered streptomycin to mice to disrupt gut microbiota.
- Measured the expression of inducible nitric oxide synthase (iNOS) in the caecal mucosa.
- Analyzed the availability of galactarate and glucarate in the murine caecum post-antibiotic treatment.
- Utilized genetic modification to ablate S. Typhimurium catabolic pathways for galactarate and glucarate.
Main Results:
- Streptomycin treatment increased iNOS expression in the caecal mucosa, leading to higher levels of galactarate and glucarate.
- S. Typhimurium utilized galactarate and glucarate in the gut lumen of streptomycin-treated mice.
- Genetic deletion of pathways for galactarate and glucarate metabolism significantly reduced S. Typhimurium competitiveness.
Conclusions:
- Host-mediated oxidation of galactose and glucose promotes post-antibiotic expansion of S. Typhimurium.
- Increased availability of galactarate and glucarate, driven by host iNOS expression, supports pathogen growth after antibiotic treatment.
- This study identifies host carbohydrate oxidation as a key mechanism in post-antibiotic pathogen expansion within the gut ecosystem.
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