New York: Treatment with good bacteria widely used in probiotic supplements can strengthen bones, especially in females, finds a study that may develop novel ways of treating bone loss condition osteoporosis.
The study showed that healthy mice fed with Lactobacillyus rhamnosus GG (LGG) bugs demonstrated an immune response that stimulated an increase in bone density.
The effect seen in young female mice is linked to a metabolite called butyrate or butyric acid — a type of fatty acid produced by gut bacteria. This in turn activated bone-enhancing immune cells, including regulatory T cells, the researchers said.
“The significance of the study is that probiotics are, at least in mice, an effective means to increase bone density,” said Roberto Pacifici from the Emory University in the US.
“Our findings will need to be validated in human studies,” Pacifici says. “If successful, this research could substantiate the use of butyrate or probiotics as a novel, safe, and inexpensive treatment for optimizing skeletal development in young people and to prevent osteoporosis in older people.”
In the study, published in the journal Immunity, the team found that oral LGG supplementation for four weeks increased bone formation in female mice by stimulating the growth of butyrate-producing gut bacteria, including Clostridia.
Supplementation with either LGG or butyrate induced the expansion of regulatory T cells in the intestine and in bone marrow — the spongy tissue inside some bones.
This caused T cells in the bone marrow to secrete a protein called Wnt10b — known to be critical for bone development. By contrast, treatments that inhibited the expansion of regulatory T cells prevented bone formation induced by LGG and butyrate, the researchers explained.
The use of probiotics or butyrate to increase the number of regulatory T cells can also be used in transplant medicine or as a treatment for inflammatory and autoimmune conditions.
Clinical trials are in progress to validate the efficacy of probiotics in humans.
[source_without_link]IANS[/source_without_link]