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Justin L. Sonnenburg

Researcher at Stanford University

Publications -  167
Citations -  24459

Justin L. Sonnenburg is an academic researcher from Stanford University. The author has contributed to research in topics: Gut flora & Microbiome. The author has an hindex of 54, co-authored 147 publications receiving 17651 citations. Previous affiliations of Justin L. Sonnenburg include University of California, Davis & Washington University in St. Louis.

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Host-Bacterial Mutualism in the Human Intestine

TL;DR: New studies are revealing how the gut microbiota has coevolved with us and how it manipulates and complements the authors' biology in ways that are mutually beneficial.
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Diet–microbiota interactions as moderators of human metabolism

TL;DR: A body of knowledge is accumulating that points to the gut microbiota as a mediator of dietary impact on the host metabolic status and the prospect of therapeutic interventions such as personalized nutrition.
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Diet-induced extinctions in the gut microbiota compound over generations

TL;DR: It is shown that changes in the microbiota of mice consuming a low-MAC diet and harbouring a human microbiota are largely reversible within a single generation, and that taxa driven to low abundance when dietary MACs are scarce are inefficiently transferred to the next generation and are at increased risk of becoming extinct within an isolated population.
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Glycan Foraging in Vivo by an Intestine-Adapted Bacterial Symbiont

TL;DR: It is found that Bacteroides thetaiotaomicron bacteria assembled on food particles and mucus, selectively induced outer-membrane polysaccharide-binding proteins and glycoside hydrolases, prioritized the consumption of liberated hexose sugars, and revealed a capacity to turn to host mucus glycans whenpolysaccharides were absent from the diet.
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Microbiota-liberated host sugars facilitate post-antibiotic expansion of enteric pathogens

TL;DR: The data show that antibiotic-induced disruption of the resident microbiota and subsequent alteration in mucosal carbohydrate availability are exploited by these two distantly related enteric pathogens in a similar manner, which suggests new therapeutic approaches for preventing diseases caused by antibiotic-associated pathogens.