From the gut to the strut: where inflammation reigns, bone abstains

J Clin Invest. 2016 Jun 1;126(6):2045-8. doi: 10.1172/JCI87430. Epub 2016 Apr 25.

Abstract

In this issue of the JCI, Li et al. show that germ-free mice, when chemically castrated, do not lose bone - a finding that unequivocally establishes a role of gut microbiota in mediating hypogonadal bone loss. Additionally and not unexpectedly, probiotics reversed hypogonadal osteopenia in sex steroid-deficient mice by preventing the disruption of gut barrier function and dampening cytokine-induced inflammation. The authors propose that TNFα is a key mediator; however, it is very likely that other molecules - including IL-1, IL-6, IL-17, RANKL, OPG, and CCL2 - modulate probiotic action. The results of this study highlight the potential for repurposing probiotics for the therapy of osteoporosis. Future placebo-controlled clinical trials will be required to establish safety and efficacy of probiotics in reducing fracture risk in people.

Publication types

  • Comment

MeSH terms

  • Animals
  • Bone and Bones
  • Inflammation*
  • Interleukin-1
  • Interleukin-17
  • Mice
  • Probiotics*

Substances

  • Interleukin-1
  • Interleukin-17