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You are here: Home / Education / E-learning / ECTS Webinar Series Bone, Muscle & Beyond / The gut-bone axis: how the gut microbiota communicates with bone

The gut-bone axis: how the gut microbiota communicates with bone

The gut-bone axis: how the gut microbiota communicates with bone

Live Webinar: 1 April 2021, 4 pm CET 

Organised by ECTS

Date & Time:  1 April 2021, 4 pm CET

Featuring Roberto Pacifici, and moderated by Lars Folkestad

Costs: Live webinar is free for ECTS members and non-members, but a registration is required. Recordings are accessible to ECTS members only.

Format:

  • 5 min welcome & introductions
  • 35 min presentation on “The gut-bone axis: how the gut microbiota communicates with bone”
  • 20 min Q&A

Learning Objectives:

  • Learn how the gut microbiota regulates the intestinal immune system
  • Learn how immune cells migrate from the gut to bone
  • Learn how bacterial metabolites regulate bone

Register for the Webinar

 

The Microbiome and Bone, Brussels, Belgium, 01-04-2021 has been accredited by the European Accreditation Council for Continuing Medical Education (EACCME®) with 1 European CME credits (ECMEC®s).

Each medical specialist should claim only those hours of credit that he/she actually spent
in the educational activity.”

Additional Live Coffee Shop: 1 April 2021, 5 pm CET

ECTS is pleased to invite you for an additional “Coffee Shop” informal discussion at 5 pm CET, right after the live webinar, in order to meet friends and colleagues with an interest in the bone field for a topical chat. If you are interested in this networking opportunity, please click on the button below to register for the Coffee Shop.

Register for the Coffee Shop

Featuring Roberto Pacifici, MD

Roberto Pacifici, MD, is the Garland Herndon Professor of Medicine and Director of the Division of Endocrinology, Metabolism and Lipids at Emory University, Atlanta GA. Dr. Pacifici received his MD in 1984 from the University of Perugia, Italy.   He completed his residency in Medicine at the same institution.  He was a fellow in Endocrinology and Metabolism in the Division of Bone and Mineral Metabolism at the Washington University School of Medicine from 1984 to 1988.  He has been member of the faculty of Washington University from 1988 to 2002 where he rose to the position of Shemberg Professor of Medicine. He has been at Emory as Division Director since December 2002.

Dr. Pacifici is an expert on the connections between the gut microbiome and bone, the mechanism of action of estrogen and PTH in bone, and one of the founders of the field of osteoimmunology and osteomicrobiology.  He has been the first to demonstrate a role for T lymphocytes in the regulation of bone metabolism in health and disease and the contribution of T cells to the mechanism of action of estrogen and PTH in bone and hemopoietic stem cells.  He is also an expert on bone densitometry and the clinical management of osteoporosis.  He has published 103 papers and 52 chapters, mostly in highly regarded journals. He serves as the Principal Investigators in 3 NIH grants.  He serves in the Editorial board of several specialty journals including “Bone” and the “Journal of Bone and Mineral Diseases”.  Throughout his career, Dr. Pacifici has been the recipient of such accolades as the National Osteoporosis Foundation Research Award in 1988, the American Society of Bone and Mineral Research Fuller Albright Young Investigator Award in 1995 the “Most Outstanding Research on the Pathophysiology of Osteoporosis Award” from American Society of Bone and Mineral research in 2003 and 2004, and the 2011 Louis V. Avioli Founder Award from the American Society of Bone and Mineral Research.  He is a member of the prestigious Association of American Physicians.

Moderated by Lars Folkestad

Staff Specialist at the Department of Endocrinology, Odense University Hospital

Associate Clinical Professor in Endocrinology, University of Southern Denmark

Senior Researcher at the Bone and Calcium metabolic diseases Unit, Endocrine Research Center, Department of Endocrinology,  Odense University Hospital.

Finished my Ph.D. Entitled Morbidity and Mortality in Osteogenesis Imperfecta in 2016 and have continued research within the bone filed.

Abstract

Division of Endocrinology, Metabolism and Lipids, Department of Medicine, Emory University, Atlanta, GA; Emory Microbiome Research Center, Emory University, Atlanta, GA

 

The gut microbiome (GM) is a key regulator of bone in health and disease. Alterations in GM composition and host responses to the GM contribute to pathologic bone loss, while changes in GM composition that prevent, or reverse, bone loss may be achieved by nutritional supplements with pre-, pro-, and post-biotics. GM has emerged has critical regulator of the activity of bone regulating hormones. In mice and humans, estrogen deficiency increases gut permeability, leading to increased translocation of bacterial products (e.g. LPS and flagellin), activation and expansion of intestinal immune cells, and migration of TNF producing T cells and Th17 cells from the gut to the bone marrow (BM). The resulting expansion of cytokine producing T cells in the BM leads to increase secretion of TNF, IL-17 and RANKL and bone loss. In mice, continuous PTH (cPTH) treatment, a model of primary hyperparathyroidism (PHPT), induces bone loss only in the presence of the Th17 cell inducing bacteria SFB in the GM. In the presence of SFB, cPTH causes the expansion of intestinal Th17 cells and their migration to the BM. Th17 cells then release osteoclastogenic cytokines that cause bone loss. Th17 cells and IL-17 production are also increased in humans affected by PHPT, suggesting a likely role of GM in the bone loss of PHPT. Intermittent PTH (iPTH) treatment, which models the bone anabolic effects of Teriparatide, is ineffective in germ-free mice or in mice treated with antibiotics, demonstrating a requirement for GM for the bone anabolic activity of PTH. Mechanistically, GM produces permissive amount of butyrate. Butyrate diffuses to the BM where it expands regulatory T cells (Tregs). Tregs induce production of the Wnt ligand Wnt10b by CD8+ T cells, leading to Wnt signaling activation and stimulation of bone formation. In conclusion, inhibition of T cell trafficking from the gut to the BM or butyrate nutritional supplementation may represent novel strategies to prevent bone loss or stimulate bone anabolism.

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