Gua Sha attenuates the pulmonary inflammation in mice infected with PR8 virus by balancing the ratio of Treg/Th17

Abstract

Background: Gua Sha, an ancient Chinese treatment which produces the pressure on the skin, is used to prevent and treat cold for thousands of years. There’re evidences to approve that it can activate immune response and reduce the inflammation. However, how it has the effect on T helper 17 cells (Th17) and regulatory T cells (Treg) is poorly understood. Here, this study aims at the relationship between the pressure-stoke in the skin and pulmonary Th17 as well as Treg in PR8-infected mice. Methods: ICR mice were randomly divided into five groups. The body weight and survival rates of all groups were monitored through the experiment. At the end of experiment, lung inflammation was detected by HE staining and the expression of Matrix metalloproteinase-9 (MMP-9) was measured by immunohistochemistry. Th17 and Treg from lung tissues was analyzed by flow cytometry. esults: Our results indicated that the survival rates of prophylactic and therapeutic group respectively showed 20% and 10% though Gua Sha treatment didn’t restore the weight-loss of PR8-infected mice. What’s more important, Gua Sha remarkably inhibited inflammatory infiltration and the expression of MMP-9 of lung tissues in infected mice ( p ＜0.05). Finally, the ratio of Treg/Th17 from lung tissues in PR8-infected mice was significantly increased as compared with control mice while Gua Sha treatment remarkably inhibited this enhancement. All these results indicated that Gua Sha has the efficacy on reducing the pulmonary inflammation in PR8-infected mice possibly via restoring the Treg/Th17 balance. Conclusions: Our findings for the first time suggest that Gua Sha exhibits a significant inhibition of inflammatory infiltration with down-regulation of MMP-9 in lung tissues from RR8-infected mice, which might be associated with the differentiation of Th17 and Treg. Further research will be carried toward how Gua Sha functions on maintaining the homeostasis of Th17 and Treg in the lungs.