Mechanisms of action of radon therapy on cytokine levels in normal mice and rheumatoid arthritis mouse model

Abstract

The typical indication of radon therapy is rheumatoid arthritis. Although there are several reports that radon therapy has regulation effects on Th17 cells, there has been no study reporting that radon inhalation affects the immune balance among Th1, Th2, and Th17. The purpose of this study is to examine the cytokine changes after radon inhalation. BALB/c mice inhaled radon at 2,000 Bq/m 3 for 2 or 4 weeks. SKG/Jcl mice inhaled radon at 2,000 Bq/m 3 for 4 weeks after zymosan administration. The results showed that radon inhalation for 4 weeks activated the immune response of Th1, Th2, and Th17. Moreover, the balance among them was not lost by radon inhalation. Radon inhalation for 4 weeks decreased superoxide dismutase activity and increased catalase activity in spleen. These findings suggest that an imbalance of oxidative stress may contribute to activate the immune response. Although zymosan administration activated Th17 immune response and decreased Th1 and Th2 immune response in SKG/Jcl mice, most cytokines related to Th1, Th2, and Th17 approached the normal level by radon inhalation. These findings suggested that radon inhalation has a different action between SKG/Jcl mice and normal BABL/c mice. This may indicate that radon inhalation has an immunomodulation function.

Immunomodulatory Effects of Radon Inhalation on Lipopolysaccharide-Induced Inflammation in Mice

“…The results for Th1- and Th17-prone cytokines may indicate that radon inhalation regulates Th1 and Th17 cell responses via Treg cell activation. We had previously reported that radon inhalation inhibits Th17 cell responses related to RA development due to the activation of Th1 and Th2 cell responses [ 11 ]. Since the results of the present study show that LPS administration produces an immune response different from that observed in RA [ 11 ], we examined how radon inhalation affects the immune response induced by LPS administration.…”

“…We had previously reported that radon inhalation inhibits Th17 cell responses related to RA development due to the activation of Th1 and Th2 cell responses [ 11 ]. Since the results of the present study show that LPS administration produces an immune response different from that observed in RA [ 11 ], we examined how radon inhalation affects the immune response induced by LPS administration. The results demonstrated that radon inhalation reduced LPS-induced inflammation by inhibiting the production of Th1- and Th17-prone cytokines.…”

“…Although zymosan administration in SKG/Jcl mice (RA mice) increased IL-6 levels and decreased IL-12(p70) and IL-4 levels, radon inhalation decreased IL-6 levels and increased IL-12 (p70) and IL-4 levels. However, the antioxidative function in the lungs did not change [ 11 ]. In addition, the duration after LPS administration may be an important factor for evaluating oxidative stress in the organs.…”

“…A report showed that the levels of Th17-related cytokines were higher, whereas the levels of Treg-related cytokines were significantly lower, in patients with RA than those in healthy individuals [ 10 ]. In our previous study, we reported differences in cytokine production between normal and RA mice following radon inhalation [ 11 ]. Radon inhalation for four weeks produced Th1-, Th2-, and Th17-prone cytokines in normal mice, whereas it produced only Th1- and Th2-prone cytokines and decreased Th17-prone cytokines in RA mice.…”

Naringenin ameliorates collagen‐induced arthritis through activating AMPK‐mediated autophagy in macrophages

“…Pro-inflammatory factors play an important role in the progression of RA. 7,8 Excessive TNF-α enhances inflammatory response, activates synovial fibroblasts, leads to synovial hyperplasia, and damages articular cartilage. 9 IL-1β induces the proliferation of synovial fibroblasts, which is closely related to joint synovial injury, and enhances the expression of cyclooxygenase-2 (COX-2) in synovial fibroblasts.…”