CCL22 miRNA modulated Th1 responses and induced therapeutic effects on OVA-induced mouse model of asthma

BACKGROUND: Allergic asthma is a chronic pulmonary disease characterized by a Th2 inflammatory response. Th-2-biased immune responses are known to play a key role in the pathogenesis of allergic asthma. In particular, the macrophage derived chemokine CCL22 is directly implicated in Th-2-associated inflammatory reactions. In this study, we investigated the immune modulation using CCL22 miRNA would be induced therapeutic effects on ovalbumin-sensitized and -challenged asthmatic mice. 

METHODS: The recombinant strain of Salmonella typhimurium expressing CCL22 miRNA (ST-miRCCL22) was prepared for in vivo knockdown of CCL22. Using an ovalbumin-induced asthma model, mice were sensitized and challenged, and then treated with ST-miRCCL22.

RESULTS: We constructed a recombinant strain of Salmonella typhimurium expressing CCL22 miRNA (ST-miRCCL22) for the in vivo knockdown of CCL22. The treatment of mice with established allergy led to attenuation of eosinophilia, Th2 cytokines and airway hyperresponsiveness. ST-miRCCL22 treatment also induced an increase in OVA-specific IFN-γ levels and in the frequency of lung inflammatory monocytes.

CONCLUSIONS: In our research, the CCL22 microRNA was treated to modulate imbalances in the disease. The CCL22 miRNA reduced Th1 immune responses and induced therapeutic effects on OVA-Induced mouse model of asthma. These results suggest that CCL22 miRNA could potentially be used as an effective therapeutic agent for treating asthma.