When she moved to her own lab, Hooper took another look at the plethora of genes that shot up in expression levels when a mouse was first exposed to gut bacteria. She chose one to study in more depth. Her lab quickly discovered that it was the gene for a protein dubbed RegIIIγ and it had a rare job for a protein: it’s an antibiotic. She’s gone on to show that RegIIIγ can kill bacteria by drilling a hole in their outer layers, allowing their contents seep out. Hooper speculates that RegIIIγ may help to shield the intestinal epithelium from the bacteria sloshing around inside the gut.

“The epithelium itself is a barrier, but you want to minimize even having bacteria attach to that,” says Hooper. “So these antimicrobial proteins, and probably many other immune molecules, likely help to set up a secondary barrier.”

In patients with inflammatory bowel disease, more bacterial cells reach the intestinal lining, indicating that the chemical barrier is inadequate—one hint toward a cause of this chronic disease.

Personalize the Gut

Though there’s a growing body of evidence that links variations in the microbiota to diseases—from Knight’s studies on metabolic syndrome to Blaser’s work on asthma and Schmidt’s colitis research—the mechanisms of these links are still too sketchy to translate them into of clinical medicine.

A 2009 paper in the Proceedings of the National Academy of Sciences by Jeremy Nicholson at Imperial College London and collaborators at the drug company Pfizer found that variations in one type of gut bacteria lead to differences in how people metabolize acetaminophen (Tylenol) and different propensities for liver toxicity. The authors proposed that “assessing the effects of microbiome activity should be an integral part of pharmaceutical development and of personalized health care.”

The concept resonates strongly with Knight. The vast variation he’s seen between individuals’ microbiomes leads him to think that gut bacteria will be targeted with drugs, or personalized concoctions of healthy bacteria, in the future.

“In terms of developing personalized medicine,” he says, “it seems like it makes more sense to develop medicines based on the microbiome, where the variation is so great, rather than on the human genome, where the variation is so little.”

For now, though, patients and doctors are stuck at the impasse between knowing (or guessing) the cause of a disease and having a treatment. Someone can blame their diabetes or inflammatory bowel disease on the churning mass of bacteria that lives inside their intestines, but there’s no magic pill to change the dynamics of that complicated world of the human microbiome.

	PAGE 1 2 3 4 5	Go Back