The role of dendritic cell in the nasal mucosal response inthe coexistence of allergic rhinitis and asthma

Many different local and systemic mechanisms have been blamed in the pathogenesis of ?united airways? concept. Common allergic triggers play role in development of both asthma and allergic rhinitis (AR) Dendritic cells (DC) that present these antigens trigger Th2 polarization. Besides their role in antigen presentation in innate immune system, DCs also influence the effector cells that migrate to the area of inflammation via the cytokines they secrete therefore determine the type of inflammation.The aim of this study was to determine the function of DCs in the immunopathogenesis of the ?united airways? concept via measuring levels of interleukin (IL)-1, IL-4, IL-6,IL-10, IL-13, IL25, interferon? (IFN?) and transforming growth faktör-ß (TGF-ß) in nasal lavaj fluid of children with only asthma, only AR and both asthma and AR and comparing these with the ones in nonallergic children.Eighty children aged between 5-17 years were enrolled in the study and evaluated in four groups as nonatopic control, atopic asthma, AR and asthma with AR. Age, gender, clinical severity and the age at initiation of these findings were recorded. Nasal lavage was performed in all children and levels of IL-1, IL-4, IL-6, IL-10, IL-13, IL-25, IFN? and TGF-ß were measured in nasal lavage fluids.Mean age of the children (39 male, 41 female) enrolled in the study was 10.0 ± 2.9 years. Levels of IL-1 were not different between the groups (p=0.379). Likewise, levels of IL-6, IL-10 ve IL-13 were similar between the groups (p=0.748, p=0.126, p=0.249 respectively). However, it was detected that levels of IL-25 were lowest in the asthma group but highest in the control group (p=0.028). On the contrary, IFN? levels were highest in the asthma group with 27.8 ± 16.4 pg/mL while lowest in the asthma with AR group (p=0.009). TGFß levels did not demonstrate a statistically significant differnece between the groups.Levels of IL-25 detected in our study might indicate that stimulation of Th2 response via upregulation of this cytokines? receptors by the DCs influence clinical outcome. Response to IL-25 might be the determinent of allergic inflammation and absence of an increase in IL-4 or IL-13 levels despite high IL-25 levels might be attributed to lack of response to IL-25. Moreover, high levels of IFN? in children with coexistent asthma and AR might be due to a more depressed Th1 response compared to the cases with either disease alone.