Microbes help produce serotonin in gut

A group of approximately 20 species of bacteria is important for the production of serotonin in the gut, according to a new study.
Although serotonin is well known as a brain neurotransmitter, it is estimated that 90 per cent of the body's serotonin is made in the digestive tract.
Altered levels of peripheral serotonin have been linked to diseases such as irritable bowel syndrome, cardiovascular disease, and osteoporosis.
Peripheral serotonin is produced in the digestive tract by enterochromaffin (EC) cells and also by particular types of immune cells and neurons.
Elaine Hsiao, research assistant professor of biology and biological engineering at California Institute of Technology, and her colleagues first wanted to know if gut microbes have any effect on serotonin production in the gut and, if so, in which types of cells.

They began by measuring peripheral serotonin levels in mice with normal populations of gut bacteria and also in germ-free mice that lack these resident microbes.

The researchers found that the EC cells from germ-free mice produced approximately 60 per cent less serotonin than did their peers with conventional bacterial colonies.
When these germ-free mice were recolonised with normal gut microbes, the serotonin levels went back up - showing that the deficit in serotonin can be reversed.
"EC cells are rich sources of serotonin in the gut. What we saw in this experiment is that they appear to depend on microbes to make serotonin - or at least a large portion of it," said Jessica Yano, first author on the paper and a research technician working with Hsiao.

The researchers next wanted to find out whether specific species of bacteria, out of the diverse pool of microbes that inhabit the gut, are interacting with EC cells to make serotonin.
After testing several different single species and groups of known gut microbes, Yano, Hsiao, and colleagues observed that one condition - the presence of a group of approximately 20 species of spore-forming bacteria - elevated serotonin levels in germ-free mice.
The mice treated with this group also showed an increase in gastrointestinal motility compared to their germ-free counterparts, and changes in the activation of blood platelets, which are known to use serotonin to promote clotting.

The researchers also identified several particular metabolites - products of the microbes' metabolism - that were regulated by spore-forming bacteria and that elevated serotonin from EC cells in culture.
Furthermore, increasing these metabolites in germ-free mice increased their serotonin levels.
The study was published in the journal Cell.