Nasal Periostin Levels and Acute Symptoms in Asthmatics During Viral-induced Exacerbations

Eighty percent of children with asthma exacerbations will have an associated viral infection. Defining the local inflammatory mediators that may lead to exacerbations can provide targets for future therapies. We hypothesized that nasal periostin is higher in exacerbating asthmatics with viral infections and that this level correlates with symptom severity during acute viral-induced exacerbations of asthma. We recruited 97 patients (exacerbating asthma n = 69, controls = 28) with upper respiratory infection symptoms from the Emergency Department. Baseline Pediatric Respiratory Symptoms (PRS) Scores were recorded. Nasopharyngeal swabs were used to detect the presence of virus by viral genome sequencing. Nasal filter paper was used to collect nasal mucosal lining fluid, and after elution, inflammatory mediators were analyzed using bead-array immunoassay. Asthmatics expressed higher nasal periostin compared to controls (means=17.37pg/mL, 5.86pg/mL respectively; p<0.05). Those asthmatics with viral infections and moderate/severe symptoms by PRS had more periostin than asthmatics with viral infections and mild symptoms (means=22.5pg/mL, 12.30pg/mL, respectively; p<0.05). Among asthmatics with moderate/severe symptoms, there was no difference between those with and without viruses. In all asthmatics, acute symptoms correlated with periostin levels (R2= 0.2, p < 0.05). Periostin levels were higher in asthmatics with personal history of allergic rhinitis (AR) compared to asthmatics without AR (means=20.19pg/mL, 4.71pg/mL, respectively; p<0.05). Nasal periostin levels are higher in asthmatics and are increased with moderate/severe symptoms during viral-induced asthma exacerbations. Nasal periostin levels likely represent host Th2 endotype rather than exposure to virus during asthma exacerbations.