University of Michigan Medical School scientists have determined common "staph" infections may cause immune-system cells in the skin to react in a way that promotes eczema.
The connection, detailed in research published in the journal Nature, may offer an explanation for what causes the red, itchy, and scaly skin condition suffered by millions of Americans. That explanation could lead to new and better treatments, the researchers said.
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"We know that 90 percent of patients with atopic dermatitis, also called eczema, have staph bacteria detectable on their skin," said Gabriel Nunez, M.D., noting genetic vulnerability likely also plays a role. "But until now, it has not been suspected that the contribution was primary, because there was not a clear mechanistic link. Now we have evidence that there may indeed be a direct link."
The new study, involving laboratory mice, found that a toxin produced by the common bacteria Staphylococcus aureus — "staph" — provokes immune-system cells to release tiny granules that cause skin inflammation, a reaction that produces eczema-like rashes.
Dr. Nunez said the finding could provide a new avenue for developing treatments to help the 15 percent to 30 percent of children, and 5 percent of adults who have eczema. The challenge now, he said, is to develop ways to inhibit the effects of delta toxin, so that mast cells don't get provoked and inflammation doesn't occur.
"This bacterium is everywhere, but very little is known about the delta toxin," Nunez explains. "The bacteria do not likely produce it to cause disease, but produce it in response to an increase in neighboring bacteria."
Some patients have noted that taking antibiotics for other conditions can produce a lessening of eczema symptoms. But antibiotics have many drawbacks, including the threat of contributing to multi-drug resistant Staphylococcus aureus, or MRSA.
The new study was funded by the National Institutes of Health.
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