(ABC4) – A new study has shed light on how obesity can change the immune system — affecting how treatments for allergies and asthma impact the body.

Researchers at the Salk Institute, Gladstone Institutes, and UC San Francisco (UCSF) teamed up to study how obesity changes the molecular underpinnings of allergic inflammation, both in mice and humans.

When mice with atopic dermatitis, a common type of allergic skin inflammation, are treated with drugs that target the immune system, their thickened itchy skin heals rather quickly. When scientists gave this same treatment to obese mice it made their skin worse.

Scientists say this new discovery can help clinicians treat allergies and asthma better in obese people.

“We’re living in an era when the rate of obesity is increasing around the world,” says Professor Alex Marson, co-senior author, and director of the Gladstone-UCSF Institute of Genomic Immunology. “Changes in diet and body composition can affect the immune system, so we have to think about how diseases that involve the immune system might differ between individuals.

Obesity is sometimes classified as a chronic inflammatory state that alters the immune system in many ways. Clinicians have reported that people with obesity often seem to have different courses of disease—from infections and allergies to cancer—and respond differently to some treatments.

When researchers analyzed the immune cells and molecules that were active in lean and obese mice, their findings revealed something different from what they had predicted.

“What we were expecting to see in the obese mice was just a greater degree of the same kind of inflammation,” says Bapat. “Instead, we saw a completely different kind of inflammation.”

The atopic dermatitis was completely different in the obese mice, raising the question of whether the drugs that work in lean animals would also be effective in obese animals.

Over the past couple of years, scientists have focused on developing drugs that treat atopic dermatitis that would be most effective in lean mice — by dampening the response of a specific cell. The only problem is that the cell is not active in obese mice.

“The treatment became a robust anti-treatment,” says Bapat. “This suggests that you can have identical twins show up to the hospital with the same disease, but if one is obese and one is lean, maybe the same drug won’t work on both.”

Although more studies on people are needed, the data hints that in humans and mice alike, obesity causes a switch in inflammation that has consequences for the pathology of allergic disease and the effectiveness of immune therapies that target those specific cells most commonly associated with inflammation.