A study published online December 15, 2013 in Nature Medicine shows that mice allowed to become obese develop specific immune system changes leading to airway hyper-reactivity. Researchers at Boston Children’s Hospital found that mice fed a high fat diet to the point of obesity experienced increases in IL-1β, interleukin 17A, ILC3 cells, and NLRP3 in lung cells, all of which can cause asthma symptoms.
Blocking production of IL-1β, IL17A, or NLRP3 in the obese mice prevented the onset of asthma symptoms. Placement of IL-1β or ILC3 cells into the lungs of the obese mice increased production of IL74 and resulted in asthma symptoms.
The researchers also looked at lung fluid obtained from asthma patients; those patients with severe asthma had more ILC3 cells and IL17 than did patients with mild or no asthma. According to the researchers, elevated levels of IL17 and IL-1β are common in obese people.
Co-lead researcher Dale Umetsu said, “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. . . . We have discovered an inflammatory pathway to asthma that previously had not been recognized. This pathway may be resistant to standard asthma medications such as corticosteroids.”
Read the Children’s Hospital press release.
Read the abstract.
