University of Texas Southwestern scientists looked at how serotonin – one of the “feel good” hormones (90% of which is actually produced in the gastrointestinal tract) – can reduce fatal intestinal infections.[i] As serotonin is such a major player in the GI system, it makes sense that it has a profound effect on the organisms that live in there: “Neurotransmitters alter gut physiology by modulating intestinal smooth muscle contraction, submucosal blood flow, barrier function, immune responses, and chloride and potassium secretion.” And of course, like everything in the gut, this is a 2 way-street in that production of serotonin (and other chemical messengers) is reliant upon the composition of the gut bacteria (and viruses as well).
The scientists grew the pathogen, E.coli 0157 (which you’ve heard of as it causes periodic outbreaks of severe foodborne illness) in their lab and exposed bacteria to serotonin. The hormone “significantly” reduced the expression of the genes used by the bacteria to cause infections. Other experiments on human cells showed that “…the bacteria could no longer cause infection-associated lesions on the cells if these bacteria were exposed to serotonin.”[ii]
They then ran tests in animals. A bacterium called Citrobacter rodentium is used in rodents to mimic E.coli infection in humans. Mice were bred to either over- or under- produce serotonin in their GI tracts, and those who over-produced were less likely to become colonized with C. rodentium when exposed, or at least, had a mild form of the illness it causes. Giving mice Prozac (fluoxetine), which increases available serotonin, also prevented the animals from getting sick when exposed to the pathogen. The mice that under-produced serotonin rapidly became sick when exposed to the C. rodentium, and frequently died.
These researchers actually identified the receptor for serotonin on both these pathogens, E. coli and C. rodentium. The receptor is a protein called CpxA, and it is found on many species of gut bacteria, of course suggesting that the hormone has profound effect on the health of the gut bacterial biome.
The lead researcher in the study suggests that it may be possible to treat bacterial infections (it turns out that Salmonella, Shigella disenteria (remember that one from this article, on phage therapy?!) , etc. also express the CpXA receptor) using serotonin medications like Prozac: “The fact that one can conceptually co-opt these drugs already used in the clinic (e.g., Prozac) to treat infectious diseases is potentially exciting.” I find that a fascinating concept in that, you have to wonder if the success of the SSRIs (selective serotonin reuptake inhibitors) for all these decades doesn’t have as much to do with their effect on the gut bacteria as with their effect on increasing serotonin in the human brain. It’s also interesting to contemplate this: since we know that stress adversely affects the gut bacteria, it’s easy again to envision this vicious cycle: stress changing the gut bacteria which changes the production of serotonin and suppresses the immune system making you more susceptible to pathogens, which in turn, changes the composition of the gut biome, etc.