Role of interleukin-23 in the development of nonallergic eosinophilic inflammation in a murine model of asthma

Abstract

Non-allergic asthma: Possible therapeutic target identified Targeting levels of a pro-inflammatory protein may help quell responses to airway irritants in patients with non-allergic asthma. Asthma often occurs when allergen exposure triggers an increase in white blood cells called eosinophils and the subsequent release of pro-inflammatory proteins such as interleukin-23 (IL-23) in the airways. However, research suggests up to one-third of sufferers have non-allergic eosinophilic asthma (NAEA), wherein airway inflammation is triggered by no specific allergen. Heung-Woo Park at the Seoul National University Medical Research Center, South Korea, and co-workers created a mouse model with excess IL-23 to examine the protein’s role in NAEA inflammation. They monitored airway responses to low doses of an acid irritant or diesel exhaust particles. The combination of high IL-23 plus an irritant triggered the release of other pro-inflammatory proteins in the airways, aggravating asthma symptoms.