Bacteria get a bad rap. Although most people wield their Lysol like a sword against these organisms, in fact, many kinds of bacteria help us survive. Now, research has revealed that select microbes might also play a key role in preventing diabetes.
The human body runs on glucose, and the hormone insulin keeps it from surging too high. Each year, about 15,000 people in the United States are diagnosed with type 1 diabetes, which strikes when their immune systems attack the cells in their pancreases, which make insulin. Researchers have spent years trying to understand what triggers this attack on the body's own cells.
Some studies have shown that mice exposed to different microbes develop type 1 diabetes at varying rates, hinting that some bacteria might help modulate early stages of the disease. But specific information about how this works, and which bacteria were important, remained elusive.
Immunologist Alexander Chervonsky of the University of Chicago in Illinois and his colleagues assessed how the microbial milieu impacts diabetes in mice. In some animals genetically susceptible to type 1 diabetes, the researchers knocked out a gene that protects against bacterial infections. The researchers then exposed five of the standard diabetes-prone mice and five of the germ-vulnerable mice to a typical environment with plenty of microbes. All of the regular mice and four of the five germ-prone mice developed diabetes, so it seemed that susceptibility to infection made no difference. But when the researchers looked for T cells, a marker of immune system activity, in different tissues, they did see significantly less T-cell activity--something that’s also a sign of incipient diabetes--in the pancreatic lymph nodes of the gene-free mice, they reported on 21 September in Nature.
Which microbes were behind the diminished T-cell activity? The researchers keyed in on a cocktail of bacteria known to inhabit the pancreatic lymph nodes normally. They placed some diabetes-susceptible mice in a germ-free environment and exposed others to only those bacteria. All the mice in the germ-free environment developed diabetes; none of the mice exposed to the bacteria showed signs of the disease.
Chervonsky's group is now examining whether mice with type 1 diabetes living in otherwise normal conditions lack these key microbes. "If we find the bacterial lineage that is protective in mice, that should be convincing enough to try in humans," he says. But he notes that researchers will have to understand exactly how these bacteria call off the immune system's attack to produce treatments for type 1 diabetes patients.
Developmental biologist Margaret McFall-Ngai of the University of Wisconsin, Madison, says the work reinforces the idea that microbes within our bodies can profoundly affect how our organs function. And although immunologist David Relman at Stanford University in Palo Alto, California, cautions against ascribing too great importance to the role of microbes in human diabetes, he does think the results are worth noting: "If nothing else, this forces us to put another variable on the table that's not been a part of the mix."