A recent animal study has allegedly identified a new immunological connec- tion between obesity and asthma involving “inflammasome activation and production of cytokine interleukin-17 by innate lymphoid cells in the lung,” according to a concurrent editorial published in Nature Medicine. Hye Young Kim, et al., “Interluekin-17-producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity,” Nature Medicine, January 2014. After studying mice that were raised on a high-fat  diet until they became obese and developed asthma, researchers with Boston Children’s Hospital apparently reported that “obesity appeared to alter the innate immune system—the body’s first responder to infection—in several ways to cause lung inflammation.” In particular, they noted that, compared with non-obese mice, “the lungs of the obese, asthmatic mice had several differences”: (i) “High levels of the protein interleukin 17A (IL17A), a cytokine (signaling molecule) associated with several inflammatory conditions”; (ii) “Increased numbers of the immune cells that produce IL17A, known as type3 innate lymphoid cells (ILC3 cells)”; (iii) “Activation of an inflammatory protein known as NLRP3 inside lung cells”; and (iv) “Increased production of the cytokine IL-1β, a stimulator of ILC3 cells.” See Boston Children’s Hospital Press Release, December 15, 2013

“The association between obesity and asthma has been known for several years, but the specific mechanisms by which obesity causes asthma have been undefined until now,” concludes the study. “We now suggest that the inflammation in obesity, which has been recently shown to arise from NLRP3 activation and excess production of cytokine IL-1β, also underlies the devel- opment of asthma that is associated with obesity.”