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Dietary amino acids regulate Salmonella colonization via microbiota-dependent mechanisms in the mouse gut

Author

Listed:
  • Joseph M. Pickard

    (University of Michigan Medical School)

  • Steffen Porwollik

    (University of California, Irvine, School of Medicine)

  • Gustavo Caballero-Flores

    (University of Michigan Medical School
    University of Wisconsin)

  • Roberta Caruso

    (University of Michigan Medical School)

  • Shinji Fukuda

    (Keio University, Tsuruoka
    Kanagawa Institute of Industrial Science and Technology
    University of Tsukuba, Tsukuba
    Juntendo University Graduate School of Medicine, Bunkyo-ku)

  • Tomoyoshi Soga

    (Keio University, Tsuruoka)

  • Naohiro Inohara

    (University of Michigan Medical School)

  • Michael McClelland

    (University of California, Irvine, School of Medicine)

  • Gabriel Núñez

    (University of Michigan Medical School)

Abstract

The gut microbiota confers host protection against pathogen colonization early after infection. Several mechanisms underlying the protection have been described, but the contributions of nutrient competition versus direct inhibition are controversial. Using an ex vivo model of Salmonella growth in the mouse cecum with its indigenous microbes, we find that nutrient limitation and typical inhibitory factors alone cannot prevent pathogen growth. However, the addition of certain amino acids markedly reverses the microbiota’s ability to suppress pathogen growth. Enhanced Salmonella colonization after antibiotic treatment is ablated by exclusion of dietary protein, which requires the presence of the microbiota. Thus, dietary protein and amino acids are important regulators of colonization resistance.

Suggested Citation

  • Joseph M. Pickard & Steffen Porwollik & Gustavo Caballero-Flores & Roberta Caruso & Shinji Fukuda & Tomoyoshi Soga & Naohiro Inohara & Michael McClelland & Gabriel Núñez, 2025. "Dietary amino acids regulate Salmonella colonization via microbiota-dependent mechanisms in the mouse gut," Nature Communications, Nature, vol. 16(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-59706-1
    DOI: 10.1038/s41467-025-59706-1
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