4.7 Review

The intestinal microbiota fuelling metabolic inflammation

Journal

NATURE REVIEWS IMMUNOLOGY
Volume 20, Issue 1, Pages 40-54

Publisher

NATURE PUBLISHING GROUP
DOI: 10.1038/s41577-019-0198-4

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Funding

  1. Excellence Initiative (Competence Centres for Excellent Technologies -COMET) of the Austrian Research Promotion Agency FFG: Research Centre of Excellence in Vascular Ageing Tyrol
  2. VASCage (K-Project) [843536]
  3. BMVIT, BMWFW
  4. Standortagentur Tirol
  5. Gilead Biosciences Fellowship
  6. Austrian Science Fund [P 29379-B28]
  7. Austrian Society of Gastroenterology and Hepatology (OGGH)
  8. European Crohn's and Colitis Organization (ECCO)
  9. Abisch Frenkel Foundation for the Promotion of Life Sciences
  10. Gurwin Family Fund for Scientific Research
  11. Leona M. and Harry B. Helmsley Charitable Trust
  12. Crown Endowment Fund for Immunological Research
  13. estate of L. Hershkovich
  14. Benoziyo Endowment Fund for the Advancement of Science
  15. Adelis Foundation - European Research Council
  16. Marie Curie Integration grant
  17. German-Israeli Foundation for Scientific Research and Development
  18. Israel Science Foundation
  19. Minerva Foundation
  20. Rising Tide Foundation
  21. Helmholtz Foundation
  22. European Foundation for the Study of Diabetes
  23. Howard Hughes Medical Institute (HHMI)

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Low-grade inflammation is the hallmark of metabolic disorders such as obesity, type 2 diabetes and nonalcoholic fatty liver disease. Emerging evidence indicates that these disorders are characterized by alterations in the intestinal microbiota composition and its metabolites, which translocate from the gut across a disrupted intestinal barrier to affect various metabolic organs, such as the liver and adipose tissue, thereby contributing to metabolic inflammation. Here, we discuss some of the recently identified mechanisms that showcase the role of the intestinal microbiota and barrier dysfunction in metabolic inflammation. We propose a concept by which the gut microbiota fuels metabolic inflammation and dysregulation.

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