Division of Endocrinology, Metabolism and Lipids, Department of Medicine, Emory University, Atlanta, United States; Emory Microbiome Research Center, Emory University, Atlanta, United States
Trevor M Darby
Emory Microbiome Research Center, Emory University, Atlanta, United States; Department of Pediatrics, Emory University, Atlanta, United States
Emory Hsu
Division of Endocrinology, Metabolism and Lipids, Department of Medicine, Emory University, Atlanta, United States; Emory Microbiome Research Center, Emory University, Atlanta, United States
Mingcan Yu
Division of Endocrinology, Metabolism and Lipids, Department of Medicine, Emory University, Atlanta, United States; Emory Microbiome Research Center, Emory University, Atlanta, United States
Division of Endocrinology, Metabolism and Lipids, Department of Medicine, Emory University, Atlanta, United States; Emory Microbiome Research Center, Emory University, Atlanta, United States
Hamid Dar
Division of Endocrinology, Metabolism and Lipids, Department of Medicine, Emory University, Atlanta, United States; Emory Microbiome Research Center, Emory University, Atlanta, United States
Jau-Yi Li
Division of Endocrinology, Metabolism and Lipids, Department of Medicine, Emory University, Atlanta, United States; Emory Microbiome Research Center, Emory University, Atlanta, United States
Jonathan Adams
Division of Endocrinology, Metabolism and Lipids, Department of Medicine, Emory University, Atlanta, United States; Emory Microbiome Research Center, Emory University, Atlanta, United States
Rheinallt M Jones
Emory Microbiome Research Center, Emory University, Atlanta, United States; Department of Pediatrics, Emory University, Atlanta, United States
Division of Endocrinology, Metabolism and Lipids, Department of Medicine, Emory University, Atlanta, United States; Emory Microbiome Research Center, Emory University, Atlanta, United States; Immunology and Molecular Pathogenesis Program, Emory University, Atlanta, United States
Genetic factors account for the majority of the variance of human bone mass, but the contribution of non-genetic factors remains largely unknown. By utilizing maternal/offspring transmission, cohabitation, or fecal material transplantation (FMT) studies, we investigated the influence of the gut microbiome on skeletal maturation. We show that the gut microbiome is a communicable regulator of bone structure and turnover in mice. In addition, we found that the acquisition of a specific bacterial strain, segmented filamentous bacteria (SFB), a gut microbe that induces intestinal Th17 cell expansion, was sufficient to negatively impact skeletal maturation. These findings have significant translational implications, as the identification of methods or timing of microbiome transfer may lead to the development of bacteriotherapeutic interventions to optimize skeletal maturation in humans. Moreover, the transfer of SFB-like microbes capable of triggering the expansion of human Th17 cells during therapeutic FMT procedures could lead to significant bone loss in fecal material recipients.
