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Obesity May Cause Asthma By Altering The Immune System

New biological targets may make asthma in people with obesity easier to treat

BOSTON, Dec. 15, 2013 /PRNewswire-USNewswire/ -- Research conducted at Boston Children's Hospital indicates that obesity might cause asthma via factors in the immune system and suggests a new way of treating asthma in obese people—who often respond poorly to standard asthma medications. The study, conducted in a mouse model of asthma and in human lung fluid, was published online Dec. 15 by Nature Medicine.

A growing body of literature links asthma with obesity, but the reason for the link has been unknown. Both conditions have become more common over the last several decades. The new study, led by Dale Umetsu, MD, PhD, and Hye Young Kim, PhD, of the Division of Allergy and Immunology at Boston Children's, explored obesity's effects on the immune system.

"Since it's been a puzzle to understand why obesity predisposes people to asthma, our goal was to find the connection between these two problems, which occur in both children and adults and to explore possible new treatments," says Umetsu.

The researchers studied mice that were fed a high-fat diet causing them to become obese. Unlike mice fed normal diets, the obese mice developed airway hyper-reactivity or constricted and twitchy airways, the predominant feature of asthma.

In the study, obesity appeared to alter the innate immune system—the body's first responder to infection—in several ways to cause lung inflammation. The lungs of the obese, asthmatic mice had several differences from those of non-obese mice:

  • High levels of the protein interleukin 17A (IL17A), a cytokine (signaling molecule) associated with several inflammatory conditions
  • Increased numbers of the immune cells that produce IL17A, known as type3 innate lymphoid cells (ILC3 cells)
  • Activation of an inflammatory protein known as NLRP3 inside lung cells
  • Increased production of the cytokine IL-1β, a stimulator of ILC3 cells.

When the obese mice were genetically altered in that they could not produce IL17A or NLRP3, they did not develop asthma. But when the same mice had IL-1β or ILC3 cells placed directly in their lungs, either was enough to spur production of IL7A and to cause asthma symptoms.

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