Abstract
Objectives: Dendritic cells (DCs) play a key role as antigen-presenting cells in allergic inflammation. It has been reported, that DCs are connected with nerve fibers in the lungs during an allergic airway inflammation. Viral infections often lead to an exacerbation in bronchial asthma, the underlying mechanism is not clear yet. In this study we investigated the effect of viral respiratory infection and steroid-treatment on the number of DCs in the vagal sensory ganglia (jugular-nodose complex (JNC)) under allergic conditions.
Methods: Using a house dust mite (HDM) model for allergic airway inflammation BALB/c, mice were exposed to HDM extract intranasally (i.n.) (25µg/50µl) for 5 consecutive days a week over 7 weeks. Humane rhinovirus serotype 1B (HRV1B) was applied i.n. in the last 3 days. Therapeutic treatment with Fluticasone propionate was performed to assess steroid efficacy.
Results:Dendritic cells were found to be closely located to neurons under physiological conditions in JNC. The percentage of DCs in relation to neurons was significantly increased in allergic airway inflammation with and without viral infection in comparison to the controls (MHCII/PGP9.5: HDM 44.1±2.0% vs. control 35.1±2.3%, p= 0.01, HDM+HRV1B 45.2±2.9% vs. control 35.1±2.3%, p= 0.02). The number of DCs in JNC was found unchanged by steroid treated animals.
Conclusion: Allergic airway inflammation causes an increase of DCs in JNC. The infection with HRV1B and the steroid-treatment have no effect on the number of DCs in JNC of HDM treated animals. The increased amount of DCs indicates that intraganglionic DCs may contribute to the pathogenesis of bronchial asthma.
- © 2014 ERS