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. 2021 Feb 19;11:620466. doi: 10.3389/fendo.2020.620466

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Copyright © 2021 Cooney, Nagareddy, Murphy and Lee

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Potential mechanisms connecting the gut to the bone. (A) A leaky gut can result in bacteria translocating to other organs such as the bone where lipopolysaccharides (LPS) are recognized by toll-like receptor (TLR) 4 on hematopoietic stem cells (HSC) and mesenchymal stromal cells (MSC). (B) Increasing the production of butyrate in the intestine promotes bone formation via an increase in the differentiation of regulatory T cells (Treg). Tregs stimulate CD8⁺ T cells to secrete Wnt10b promoting the differentiation of osteoblasts and bone formation. (C) An expansion of T Helper (T_H) 17 cells in the gut can result in the migration of T_H17 cells to the bone. Additionally, the upregulation of the chemoattractant CCL20 in the bone marrow can aid the migration of intestinal T_H17 cells to the bone where the production of interleukin (IL) 17 can promote the differentiation of osteoclasts thereby promoting bone destruction.