Our modern day view of our bodies has changed quite drastically over the last century. With increased medical knowledge and the ability to detect ever-smaller and rarer life, we have continuously advanced our awareness of the world beyond that which even science fiction could have envisioned in the early 1900s. Our appreciation of life has evolved from the quaint early 20 th century belief that our bodies are pristine and pure vessels of life that are occasionally invaded by malevolent unseen forces of evil. In this modern era, we are coming to grips with the knowledge that we are fortunate symbionts, providing an ideal environment for unseen and untold communities of bacterial life who in return work tirelessly to keep us sustained, stable and productive.

As the host, it is our responsibility to maintain the proper and healthy living conditions that our bacterial tenants require. That primarily means providing timely nourishment; and our body is constructed in such a manner to remind us, like the blinking of a “low fuel” light in a car, when we need to eat or drink. As long as we are healthy, this system works and has worked spectacularly for millions of years! But when we get really sick, when our system is either severely compromised or invaded and plundered by rogue bacteria and viruses, it can be the equivalent of a Chicxulub crater-like meteor impact on the biodiversity of life within our bodies.

However, even in situations that aren’t as dire as all that, in those times when we are plagued only by the more routine dilemmas of life like the common cold, our internal stability can be compromised, albeit to a somewhat lesser extent. Throughout the millennia, our bodies have developed their systems of emergency response. One of those responses is the temporary reallocation of energy demand. When we get sick, our bodies press all available resources into fighting the infection. Consequently, that also means that our bodies aren’t worrying about finding or ingesting food. That’s a great, short-term solution…just like temporarily pulling in army reserves to bolster troops in times of need.

Just like in a prolonged war, though, that doesn’t work so well in the event of a long-term infection. Without regular and continued nourishment, the bacteria that are helping to fight the infection starve and die off, unbalancing our delicately bacterial ecosystem or allowing the existing infection to gain traction. Neither is ideal, and it makes sense that our bodies would have accounted for such an annoying dilemma with its usual flare of resourcefulness and grace. Featured in this October's issue of Nature, Joseph Pickard and Alexander Chervonsky illustrate the novel way in which mice bodies handle a similar situation.

In an ensuing infection, gut microbes need to eat even as the body is forced into starvation mode. So the body utilizes a unique system that adds a fucose sugar onto globules of fats and proteins that the bacteria can use for nourishment in times of stress. It’s not ideal and is probably similar to a military MRE (Meal Ready-to-Eat) in terms of deliciousness, but it gets the job done. In order to generate that microbial MRE, the body uses Interleukin-22 (IL22) inside of intestinal epithelial cells to express the Fut2 gene. As proof of its nourishing ability, when mice that were genetically bred to lack the Fut2 gene were stressed with a simulation of an infection, they required an extra day to return to their normal weight than the control mice.

Pickard stated in the article, the mouse fitness could either be related to decreased pathogen burden (aka resistance) or increased pathogen tolerance. To prove their hypothesis, they measured the abundance and activity of the C. rodentium bacterial infection from each test group of mice using a GoldBio L-fucose substrate called 4-Methylumbelliferyl fucopyranoside (Cat # M-580). There was no difference in the pathogen loads between the test and control groups, which showed that the Fut2 expression most likely provides beneficial tolerance as opposed to resistance to infection.

Interestingly, Pickard also noted that there is a very similar pathway that regulates antimicrobial proteins and acts as a resistance mechanism inside the body. So perhaps tolerance and resistance goes hand in hand after all. Regardless, the entire story is shaping up to be a fascinating situation and one that definitely needs further investigation. For instance, the genetic deletion of the Fut2 gene happens in 1 out of every 5 people. Fut2 has also been associated with the inflammatory bowel disorder, Crohn’s disease. Crohn’s is a terrible disease that can affect any part of the GI tract and is a life-long, debilitating condition. Crohn’s disease also happens to be genetically predisposed to run in families.

There might not be a direct link to humans yet. But it may be that without the beneficial Fut2 gene, and the timely delivery of fucose nutrients to our microbial partners, our beneficial bacteria cannot survive in the wake of intestinal infection, their loss leading to more severe physical repercussions and disabilities that otherwise might be mitigated in a healthy individual. One thing is for certain, in sickness or in health, our very lives and the quality of those lives depend on a relationship we have with organisms we cannot see, creatures we do not know, and life of which we are just now becoming aware.

I can only imagine what amazing things we will learn throughout the next century of science!

Pickard, J. M., Maurice, C. F., Kinnebrew, M. A., Abt, M. C., Schenten, D., Golovkina, T. V., ... & Chervonsky, A. V. (2014). Rapid fucosylation of intestinal epithelium sustains host-commensal symbiosis in sickness. Nature.

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