Format

Send to

Choose Destination
Calcif Tissue Int. 2018 Apr;102(4):415-425. doi: 10.1007/s00223-017-0331-y. Epub 2017 Sep 30.

Gut Microbiota, Immune System, and Bone.

Author information

1
Gerontology and Bone Metabolic Diseases Section, Department of Medical Science, University of Torino, CorsoDogliotti 14, 10126, Turin, Italy. patrizia.damelio@unito.it.
2
Gerontology and Bone Metabolic Diseases Section, Department of Medical Science, University of Torino, CorsoDogliotti 14, 10126, Turin, Italy.

Abstract

The gut microbiota (GM) is the whole of commensal, symbiotic, and pathogenic microorganisms living in our intestine. The GM-host interactions contribute to the maturation of the host immune system, modulating its systemic response. It is well documented that GM can interact with non-enteral cells such as immune cells, dendritic cells, and hepatocytes, producing molecules such as short-chain fatty acids, indole derivatives, polyamines, and secondary bile acid. The receptors for some of these molecules are expressed on immune cells, and modulate the differentiation of T effector and regulatory cells: this is the reason why dysbiosis is correlated with several autoimmune, metabolic, and neurodegenerative diseases. Due to the close interplay between immune and bone cells, GM has a central role in maintaining bone health and influences bone turnover and density. GM can improve bone health also increasing calcium absorption and modulating the production of gut serotonin, a molecule that interacts with bone cells and has been suggested to act as a bone mass regulator. Thus, GM manipulation by consumption of antibiotics, changes in dietary habits, and the use of pre- and probiotics may affect bone health. This review summarizes evidences on the influence of GM on immune system and on bone turnover and density and how GM manipulation may influence bone health.

KEYWORDS:

Bone; Gut microbiota; Immune system; Inflammation; Osteoporosis; Probiotics

PMID:
28965190
DOI:
10.1007/s00223-017-0331-y

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center