PT - JOURNAL ARTICLE AU - Maaike de Vries AU - Irene H. Heijink AU - Laura Hesse AU - Antoon J.M. van Oosterhout AU - Martijn C. Nawijn TI - Pim1 kinase affects allergic asthma in a HDM-driven mice model DP - 2014 Sep 01 TA - European Respiratory Journal PG - P1024 VI - 44 IP - Suppl 58 4099 - http://erj.ersjournals.com/content/44/Suppl_58/P1024.short 4100 - http://erj.ersjournals.com/content/44/Suppl_58/P1024.full SO - Eur Respir J2014 Sep 01; 44 AB - Allergic asthma is characterized by airway inflammation, remodelling and hyperreactivity (AHR) and it has been hypothesized that disruption of the epithelial barrier plays a key role in its pathogenesis. Since it is known that Pim1 kinase is important for eosinophil survival and we previously observed a decrease in epithelial barrier function of airway epithelial cells upon inhibition of Pim1 kinase activity, we aimed to further explore the role of Pim1 kinase in the development of allergic asthma.Pim1-deficient and wild-type control mice were intranasally sensitized with house dust mite (HDM) or PBS for 5 weeks, where after the AHR upon metacholine challenge was measured with flexivent. BAL fluid and blood was collected and cellular composition in the BAL fluid was determined. Furthermore, the levels of IL-5, IL-10, KC and IgE were measured by ELISA.Both groups of mice sensitized with HDM developed significant AHR compared to PBS-treated mice, which was independent of genotype. Analysis of the inflammatory cells in BAL fluid showed an increase in inflammatory mononuclear cells and eosinophils in the HDM sensitized mice, though the number of eosinophils showed a trend towards decreased numbers in the Pim1-deficient mice. Interestingly, a significant increase in IL-5, IL-10, KC and IgE was observed in the HDM sensitized Pim1-deficient mice compared to their wild-type counterparts.In conclusion, although we could not determine differences in AHR in the absence of Pim1 kinase activity, the observed increase in the cytokine levels indicates a divergent role for Pim1 kinase in regulating the inflammatory cytokine response versus eosinophilic inflammation in allergic asthma that should be further investigated.