Majie Cataplasm Promotes Th1 Response to Fight against Asthmatic Th2 Inflammation through NKs.

BACKGROUND

Immune cells are tightly bound up with the pathogenesis of asthma. Besides T cells, B cells, macrophages, and mast cells, the mechanism of innate lymphoid cells (ILCs) in asthma is gradually explicit. As a kind of traditional Chinese medicine, Majie cataplasm realizes its potential in the clinical setting as an adjuvant for asthma. In our previous experiments, Majie cataplasm inhibits the increasing Th1 and Th2 in allergic asthma inflammation and reshapes a balance between Th1 and Th2. As ILCs are the reflection of Th cells in lung tissues, we will figure out whether Majie cataplasm could have similar effects on ILCs or not.

METHODS

A total of 40 female C57/BL6 mice were randomly divided into the control group ( = 10), the asthma model group ( = 10), the dexamethasone group ( = 10), and the Majie cataplasm group ( = 10). Except for the control group, mice were sensitized with ovalbumin (OVA) and excited to establish mice models of asthma. Lung tissue and splenic tissue were collected at 24 h after the last challenge with OVA, and the cell suspension of the lungs and spleen was prepared. The number of ILC1s, ILC2s, ILC3s, and NKs cells in the lungs and Tregs and B10s in the spleen were detected by flow cytometry (FCM). This was followed by simultaneous quantitative detection of 40 inflammatory cytokines and chemokines in the lung by a protein microarray.

RESULTS

The dexamethasone and Majie cataplasm could restore the number of ILC1s, ILC2s, and ILC3s in lung tissue. Compared with the control group, these cells remained unchanged in the asthma model group, while ILC1s ( < 0.001, < 0.01), ILC2s ( < 0.001, < 0.01), and ILC3s ( < 0.01, < 0.05) were restored after the intervention of dexamethasone and Majie cataplasm. The number of NKs was low among the control group, the asthma model group, and the dexamethasone group, while the number of NKs rocketed in the Majie cataplasm group ( < 0.0001). For splenic Tregs and B10s, Majie cataplasm could curb the increasing numbers of them in the asthma model group ( < 0.0001, < 0.01), while only Tregs were suppressed by the dexamethasone ( < 0.0001). For the inflammatory cytokines in the lung, the contents of TNF-, TNFR2, CXCL-9, CCL-12, CCL-9, CCL-2, and CCL-5 in the asthma model group were higher than those in the control group, while the contents of GM-CSF and IL-1 were decreased. Comparing the asthma model group to the dexamethasone group, the levels of G-CSF, CCL-9, CCL-5, and TNFR2 in the former group were higher. The levels of TNF-, TNFR2, and CCL-9 in the asthma model group increase, while the levels of IFN-, IL-1, ICAM-1, and IL-4 increased in the Majie cataplasm group, especially IFN- and IL-1.

CONCLUSION

Both the dexamethasone and Majie cataplasm could control the asthmatic inflammation by reducing the inflammatory factors, inhibiting the adaptive inflammation reaction in the latter stage of inflammation and furtherly reversing the inhibition of ILC2s, ILC2s, and ILC3s. In addition, Majie cataplasm can promote the quantity of NKs and the content of IL-1 and IFN-, induce IFN- NKs to shut down the Th2 response, and tend to elicit the Th1 response.