Gut microbiota that impairs normal skeletal growth identified.
Containing a mini-ecology of its own, the human gut contains trillions of bacteria, known as the microbiota, a symbiotic entity crucial for digesting food and regulating the immune system. Gut microbiota also regulates immune processes influencing normal skeletal growth and maturation. This has led to confusion pertaining to the influence of specific microbes on immune-based osteoregulation.
Microbes needed for bone health
Now, a study from researchers at MUSC Health identifies specific microbes that play a part in the regulation of normal skeletal growth and maturation. The team states their data shows segmented filamentous bacteria (SFB) elevated the response of immune cells in the gut and liver which led to increased osteoclast activity and decreased osteoblast activity, impairing bone mass accrual in mice. The study is published in the Journal of Bone and Mineral Research Plus.
Previous studies show the post-pubertal phase of skeletal development is the critical window of plasticity supporting the formation of approximately 40% of a person’s peak bone mass. SFB has been shown to activate TH17 cells in an interleukin-17A (IL-17A) immune response effect in bone marrow and the liver, believed to have pro‐catabolic/anti‐anabolic actions in the skeleton.
Recent studies from the lab showed the gut microbiome heightens immune responses in the liver and bone environment, which impairs skeletal bone mass. The current study aims to link these aspects of SFB-mediated immunity to determine if specific gut microbes have the ability to affect skeletal health.
The current study compares germ-free mice to an SFB-colonized microbiota mouse model to show the effects of SFB and the gut microbiome on skeletal health. Results show mice with SFB microbiotic colonies exhibited a 20% reduction in trabecular bone volume, the type of bone noted for undergoing high rates of bone metabolism. Data findings show SFB-colonized mice have increased IL-17A levels in the gut and circulation and enhanced osteoclast potential.
Microbiota regulates bone growth
Results show SFB presence in gut microbiota stimulates hepatic immunity, upregulating pro-inflammatory immune factors in the liver and increasing TH17 cells in the liver draining lymph nodes. Data findings show SFB-colonization increases circulating levels of IL-17A and Lipocalin-2, an antimicrobial peptide influencing bone metabolism, both of which support osteoclast activity and suppress osteoblast activity. The group states their data shows SFB plays a critical role in regulating the immune response in both the gut and liver which has significant effects on the skeleton.
The team surmises they have identified the specific microbes responsible for impacting gut microbiota to regulate normal post‐pubertal skeletal growth and maturation. For the future, the researchers state if a way is found to prevent the colonization of SFB in the microbiome, there may be potential to optimize bone mass accrual during post-pubertal skeletal development.
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