Good Gut Microbes: Studies Explore How 'E. Faecium' Fights Off Infection

We hear a lot more about our bad bugs than our good bugs — about treatment-resistant gonorrhea and C. difficile and run-amok E.coli. But we also hear more and more about how our bodies are ecosystems where our trillions of microbes are valuable elements, worthy of cultivating.

Two papers just out in Science journals dig in to the virtues of what sounds like a helpful microbe: E. faecium, a bacterium that can actively protect our guts from infection. The research pinpointed a key enzyme in cultures of the microbe, called SagA, and found it boosted resistance to a nasty Typhoid-like pathogen in mice and worms.

I asked Dr. Emeran Mayer, author of "The Mind-Gut Connection," what to make of these new findings. Is E. faecium a gut hero, and how long before it's marketed in yoghurt? His explanation:

There are two views on the way our gut microbes play a role in defending us against pathogenic bacteria and infections:

• The ecological view, which implies that the diversity, stability and resilience of the gut microbial ecosystem is the main factor that protects us from pathogens.

• The classical microbiology view, which implies that a single microorganism and a single molecule produced by this organism is responsible for the protection against a pathogen.

A third view is sort of a hybrid of both: It postulates that there are certain microbes within a ecosystem, so-called 'keystone species,' that are closely connected to a large number of other, less important microorganism.

These keystone species play a much greater role in the overall function of the microbiome than any of the others. The two papers largely adhere to view #2, implicating a particular microbial species, E. faecium, and its metabolite SagA as a unique organism that can protect the gut and the organism (worms) from the ill effects of pathogenetic invasion by micro-organisms (Salmonella species) that can cause typhoid fever.

Most interesting, and with the most intriguing therapeutic implications, the authors transferred SagA into a common human probiotic, Lactobacillus plantarum, and administered the genetically engineered bacteria to mice, which then got the same protective effect against infection.

The goal of genetically manipulating common probiotics which have little health benefit by themselves into “factories” of pharmaceuticals with pharmacological effects on the host is being pursued by many laboratories. For example, just as SagA-producing probiotics may confer protection against bacterial infections, microbes producing short-chain fatty acids or the anti-inflammatory interleukin 10 could yield health benefits for gut inflammation.

Similarly, microbes producing the amino acid GABA may prove able to alleviate anxiety; microbes producing serotonin in the gut may have antidepressant effects; and metabolites produced by the bacterium B. fragilis may have therapeutic effects for autism spectrum disorders. All this remains to be seen.

Despite the excitement stimulated by these two publications, we have to keep the ecological view in mind: The human gut microbial ecosystem may respond in unexpected ways to a newly introduced organism or its products. Also, the pathogen may find ways around the protective effects of probiotics that produce SagA.

Still, the headline of the paper's summary describes a promising avenue: "Using microbes to fight microbes."