Looking Closer at the Role of Microbiome: Jack Gilbert and Colleagues Study Bacteria’s Broad Influence

There’s a story that Assoc. Prof. Jack Gilbert, a microbial ecologist at UChicago 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, the Sara and Harold Lincoln Thompson Professor of Surgery, 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.” Read more here

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