The gut microbiota regulates bone mass in mice

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  • Klara Sjögren
    Centre for Bone and Arthritis Research, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden
  • Cecilia Engdahl
    Centre for Bone and Arthritis Research, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden
  • Petra Henning
    Centre for Bone and Arthritis Research, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden
  • Ulf H Lerner
    Department of Molecular Periodontology, Umeå University, Umeå, Sweden
  • Valentina Tremaroli
    Center for Cardiovascular and Metabolic Research/Wallenberg Laboratory, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden
  • Marie K Lagerquist
    Centre for Bone and Arthritis Research, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden
  • Fredrik Bäckhed
    Center for Cardiovascular and Metabolic Research/Wallenberg Laboratory, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden
  • Claes Ohlsson
    Centre for Bone and Arthritis Research, Institute of Medicine, Sahlgrenska Academy at University of Gothenburg, Gothenburg, Sweden

説明

<jats:title>Abstract</jats:title> <jats:p>The gut microbiota modulates host metabolism and development of immune status. Here we show that the gut microbiota is also a major regulator of bone mass in mice. Germ-free (GF) mice exhibit increased bone mass associated with reduced number of osteoclasts per bone surface compared with conventionally raised (CONV-R) mice. Colonization of GF mice with a normal gut microbiota normalizes bone mass. Furthermore, GF mice have decreased frequency of CD4+ T cells and CD11b+/GR 1 osteoclast precursor cells in bone marrow, which could be normalized by colonization. GF mice exhibited reduced expression of inflammatory cytokines in bone and bone marrow compared with CONV-R mice. In summary, the gut microbiota regulates bone mass in mice, and we provide evidence for a mechanism involving altered immune status in bone and thereby affected osteoclast-mediated bone resorption. Further studies are required to evaluate the gut microbiota as a novel therapeutic target for osteoporosis. © 2012 American Society for Bone and Mineral Research.</jats:p>

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