Microbial Me: A Look Inside Microbiome Research

Scientists performing microbiome research are discovering how microbes not only make us sick, but also keep our bodies working.


| Winter 2015



The cities we build, the buildings we work in, the food we eat, the homes we keep, the environments where we live our lives and raise our children—all these factors affect the microbes living inside us, which in turn, scientists are discovering, can influence everything from obesity to Alzheimer’s to asthma.

Illustration by Flickr/Omnos

There’s a story that Jack Gilbert, a microbial ecologist at the University of Chicago and Argonne National Laboratory, likes to tell about a bacterium called Enterococcus faecalis. It’s sort of a love story gone wrong. Squat and vaguely jellybean-like, measuring about three microns long, E. faecalis lives in the human gastrointestinal tract. Under normal circumstances, the relationship is friendly. It’s close. It’s what microbiologists call commensal, a term whose Latin etymology conjures up togetherness and a shared dinner table. “In its original state, just living inside your gut, this bug is totally harmless,” Gilbert says. “In fact, it’s beneficial. It helps train your immune system.” Your body wants it there, needs it there, has evolved to live with it. “It’s a natural part of your gut’s flora, your ecosystem.”

All that can change, though, when a person goes in for gastrointestinal surgery. Like, for instance, to remove part of the colon and stitch the remaining pieces back together, a routine treatment for colon cancer. Afterward, some patients develop what’s called an anastomotic leak. The seam where the bowel has been rejoined breaks open, and fluids from the intestine begin seeping into the body. It’s a rare complication, but it can be disastrous, sometimes fatal. Even after years of increasingly better materials—glues, staples, stronger stitches—and increasingly precise surgical techniques, anastomotic leak persists. Some surgeons opt to avoid the risk altogether by performing a colostomy that, unpleasantly, diverts fecal matter into an external bag.

The culprit, it turns out, is usually not the stitches or the surgeon; instead, it’s a particular strain of the otherwise commensal E. faecalis. In a study published this past May, Gilbert and John Alverdy, found that the bacterium creates small holes in the intestine at the surgical site, degrading the tissue and weakening the connection. In rats with anastomotic leaks, the abundance of E. faecalis ballooned 500-fold. “It becomes like a swarm of locusts,” Gilbert says of the microbe. “And it swarms directly to the site of damage in the cell wall, grabs hold of it, and starts to break down the collagen that the body is trying to use to repair the cell damage. It’s like going to the scaffolding on a new building and just ripping it apart. And the building falls down.”


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But why? What makes this friendly bug turn against its host? The answer, Gilbert says, underlines an increasingly inescapable need to reimagine the way medicine is practiced. Not just surgery, but all medicine. And—now that he’s talking about it—not just medicine, but modern life more broadly. The cities we build, the buildings we work in, the food we eat, the homes we keep, the environments where we live our lives and raise our children—all these factors affect the microbes living inside us, which in turn, scientists are discovering, can influence everything from obesity to Alzheimer’s to asthma.

So here’s what that colorectal surgery looks like to the microbe. When the patient comes to the hospital, the first thing doctors do is blast the intestine with radiation, to kill as much bacteria as possible. Then they pump in intravenous antibiotics to try to get rid of whatever remains. “Again, it doesn’t kill everything, but, again, it creates an incredibly hostile ecosystem,” Gilbert says. Then the surgery. Doctors cut open the colon, flooding the normally anaerobic gut with oxygen. “The oxygen makes the surviving anaerobic organisms panic,” Gilbert says. “It’s like poison gas.” Finally, doctors seal up the incision and the wound begins to heal itself, siphoning nutrients, namely phosphorus, from the intestine. Suddenly there’s not enough food for the microbes.

Gilbert is excited now, waving his arms a bit, shaking the air in front of him. He’s at a Starbucks down the street from his office, gulping down black tea before his next lecture. “Let’s look at it from the bacterium’s perspective,” he says. “It’s the last of its kind, right?” Having survived radiation, antibiotics, and oxygen exposure—and along the way having likely been selected for a mutation that transforms it into a hardier strain of bug—E. faecalis now finds itself robbed of phosphorus and starving to death. “It’s like, ‘Oh my god, this is a horrible environment!’ So this bacterium, he’s normally your friend, right, but what do you think it does?” Gilbert asks. “It turns on mechanisms and pathways inside itself for nutrient acquisition.” And the best place to find those nutrients? “This lovely, nicely available healing-up area where the body’s sucking up all the phosphorus.” So that’s where the bug goes, and it attacks the wound. “And we call that an infection; we call that a pathogen. And we try to kill it off, without realizing what we did to make that pathogen appear.”