John Hopkins Researchers Discover Underlying Immune Mechanism in Eczema

“We don’t really know what causes atopic dermatitis and there aren’t many good treatments for it,” says Lloyd Miller, M.D., Ph.D., associate professor of dermatology at the Johns Hopkins University School of Medicine.

Cell Host & Microbe magazine reports some insightful information about eczema –

  • Eczema patients skin cells ‘may’ be overreacting and inflamed due to a toxin-producing bacteria on the outer-most layer of the skin.
  • Specifically a protein on our skin is in defense mode, causing our skin to think its under attack.
  • 90% of eczema sufferers have a greater chance of S. aureus bacteria (Staph) on our skin, because it’s prone to be inflamed.
  • IL-36 – may be the key to discovering how bacteria triggers inflammation

Ninety percent of patients with eczema have exceedingly high numbers of S. aureus bacteria on their inflamed skin.” Miller

Experimentation – Researchers tested their theory on mice with two different groups. One group of mice had normal skin, the others were genetically engineered to lack IL-36. As they applied gaze soaked in S. aureus to their skin, they discovered some important factors. The ‘normal mice’ developed scaly and inflamed skin. However, the genetically ‘engineer mice’ had no reaction.

What does this means? Well, they can take drastic measures to innovate medicine that gets to the root of the problem, instead of just treating the surface. *Hopefully*

“We are very excited about these results as there is currently only a single biologic treatment targeting an inflammatory mechanism in atopic dermatitis on the market. As there are patients who don’t respond or have treatment failures, it would be better if there were biologics on the market that target alternative mechanisms involved in skin inflammation,” says Miller.

They also note that untreated eczema leads to other dangers issues, such as allergies (yup!), asthma and possibly even conjunctivitis!


Leave a Reply

Your email address will not be published.