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INTRODUCTION Animal studies, and in vivo inoculation with rhinovirus, have shown that the epithelial-derived cytokine interleukin-33 (IL-33) is a major contributor to Th2-inflammation in acute asthma. However the link between IL-33 and Th2-inflammation has never been shown in naturally occurring cases of acute asthma. AIMS AND OBJECTIVES To determine whether IL-33 plays a role in driving Th2-inflammation in hospitalised acute asthma patients, we aimed to investigate whether the level of IL-33 in the nasal epithelium correlated with levels of Th2 cytokines in upper and lower airways. METHODS Patients admitted to hospital with an acute asthma exacerbation were recruited. Nasal swabs were used to sample nasal fluid representing upper airways, and induced sputum were collected, representing lower airways. Sampling was repeated after 4 weeks, and all samples analysed using Droplet Digital PCR for IL-33, IL-5 and IL-13. RESULTS Nineteen patients were recruited. Nasal IL-33 correlated with IL-5 in both upper and lower airways during acute asthma (0.75, p=0.008 and 0.74, p=0.010, respectively). Similar correlations were found with IL-13 (0.64, p=0.018 and 0.65, p=0.017, respectively). These associations were not significant at the 4-week follow-up. Sputum IL-33 was not associated with IL-5 or IL-13 in either sputum or in the nasal epithelium. CONCLUSION Nasal, but not sputum IL-33 is associated with Th2-promoting cytokines IL-5 and IL-13 in naturally occurring acute asthma cases. These findings support the role of IL-33 as an initiator of Th2-inflammation in acute asthma.