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A1424 - Presence of IL-36γ (IL1F9) in Bronchoalveolar Lavage in Patients with Asthma
Author Block: S. R. White1, D. K. Hogarth2, E. T. Naureckas1, B. Laxman3, J. Solway4, A. I. Sperling5; 1Univ of Chicago Hosp, Chicago, IL, United States, 2University of Chicago, Chicago, IL, United States, 3Medicine, Univ of Chicago Hosp, Chicago, IL, United States, 4Univ of Chicago, Chicago, IL, United States, 5Medicine/PCCM, University of Chicago, Chicago, IL, United States.
IL-36γ is a product of airway epithelial cells and can be induced by inflammatory stimuli, cytokines and environmental stressors. In mice, IL-36γ elicits neutrophilic airway inflammation. However, its role in asthma is unclear. We examined IL-36γ expression and abundance in endobronchial brushings and BAL fluid in 29 control subjects and 94 patients with mild to severe asthma, all over age 18. Subjects with asthma had a higher proportion of subjects with a history of clinical sinusitis and gastroesophageal reflux disease, lower FEV1 as percent predicted, higher absolute numbers of peripheral blood eosinophils, and a higher proportion of BAL eosinophils. IL-36γ expression above background was noted in every control and asthmatic EB sample. There was no significant difference in IL-36γ expression in airway epithelial cells obtained by EB in asthmatic compared to non-asthmatic subjects. IL-36γ protein concentrations in BAL fluid above the limit of detection in the ELISA assay could not be demonstrated in 8 of 29 (28%) of control and 46 of 94 (49%) of asthmatic BAL fluid samples. The concentration of IL-36γ protein was not significantly increased in asthmatic compared to non-asthmatic BAL fluid. For both gene expression in EB and concentration in BAL fluid, no differences were noted based on gender, age, race, step diagnosis, or FEV1 as percent predicted. Using thresholds calculated from the control subjects for high versus low numbers of absolute number of peripheral blood eosinophils, fraction of exhaled nitric oxide (FeNO), and relative proportion of either neutrophils or eosinophils in BAL fluid, while modest differences were apparent for gene expression and ELISA concentration in BAL fluid in asthmatic subjects for each parameter, none reached statistical significance. Recent data have suggested that IL-36 cytokines have a pathogenic role in psoriasis and other skin disorders. While it is tempting to suggest that epithelial-derived IL-36γ may have a role in airway inflammation in asthma, our study suggests that IL-36γ expression in these cells, and the presence of the cytokine in airways, is little different compared to non-asthmatic airways. While future studies may suggest potential activities of this cytokine in lung inflammation, we are unable to substantiate its differential expression in the airways of subjects with mild to severe asthma.