Serotonin-producing lactobacilli promoting intestinal transit
Certain strains of intestinal lactobacilli—Limosilactobacillus mucosae and Ligilactobacillus ruminis—produce bioactive serotonin that may contribute to intestinal health, improving colonic neuronal density and normalizing transit.
Lay public section
Find here your dedicated section
About this article
Serotonin is essential to the digestive system: it regulates essential gastrointestinal functions (peristalsis, vasodilation, visceral sensitivity) and promotes the development and maintenance of the enteric nervous system. Although serotonin production is mainly endogenous (in two stages: tryptophan -> 5-HTP -> serotonin), certain human enteric bacteria are suspected of contributing to it. Scientists have recently identified these bacteria and evaluated the physiological activity of this microbial serotonin on colonic innervation and intestinal motility.
95% Approximately 95% of the body's serotonin pool comes from the intestine, where it is synthesized, stored, and released by enterochromaffin cells.
Serotonin-producing lactobacilli
The results confirm that the gut microbiota synthesizes serotonin and contributes to intestinal levels of this substance: in vitro (anaerobic cultures), the human fecal microbiota of healthy volunteers produces serotonin; in vivo, serotonin is found in the stools of mice that are genetically incapable of synthesizing it once they are given microbiota. Which bacteria are responsible? Researchers have identified a pair of serotonin-producing lactobacilli (named Ls), consisting of Ligilactobacillus ruminis and Limosilactobacillus mucosae. Ls does not produce 5-HTP or serotonin from tryptophan (step 1 of synthesis), but produces serotonin in the presence of 5-HTP (step 2). This step 2 of decarboxylation of 5-HTP to serotonin requires the simultaneous presence of both bacteria in the consortium.
Effects of intestinal colonization by the bacterial duo
In axenic mice unable to produce endogenous serotonin, colonization by Ls strains alone increases entero-serotonin levels, promotes colonic innervation, and increases the number of serotonin-immunoreactive neurons. However, serum serotonin levels in mice are unchanged, suggesting that bacterial serotonin primarily regulates local intestinal functions.
The isolated Ls community produces serotonin in vitro. However, this effect is not reproduced in culture conditions with pure strains (L. mucosae or L. ruminis) or with their reconstituted co-culture, whereas this co-culture increases fecal serotonin in vivo. This suggests that microbial serotonin production may depend on specific intestinal conditions (substrates, pH, oxygen, cofactors, microbial interactions).
Enterochromaffin cells in mammals synthesize serotonin in two steps from the aromatic amino acid tryptophan (Trp):
1. Hydroxylation of Trp produces the serotonin precursor 5-hydroxytryptophan (5-HTP). Tryptophan hydroxylases (TPH), belonging to the larger family of aromatic amino acid hydroxylases (AAAH), carry out this first, rate-limiting step in serotonin synthesis.
2. 5-HTP is then decarboxylated by aromatic amino acid decarboxylases to form serotonin.
Restoring patients' intestinal motility?
Finally, Ls normalizes intestinal transit time in axenic mice. However, in patients with irritable bowel syndrome, the fecal abundance of L. mucosae (but not L. ruminis) is significantly lower than in healthy controls. And the less this bacterium is present, the harder the stools are. Could a mechanism linked to the microbiota affect local serotonin biosynthesis and intestinal motility in these patients? According to the authors, future research could determine whether these serotonin-producing bacteria are capable of restoring physiological serotonin levels in patients with intestinal motility disorders.
