Proteomic profiling of mouse lungs after radon inhalation and lipopolysaccharide administration

Radon therapy alleviates the symptoms of autoimmune diseases by enhancing antioxidant and anti-inflammatory effects. Although radon inhalation normalizes serum cytokine concentrations modulated by lipopolysaccharide (LPS) administration, it also increases pulmonary oxidative stress. Hence, its effects on lungs must be comprehensively evaluated; however, no study has reported the effects of short-term radon inhalation or the associated proteomic changes. In this study, we aimed to evaluate the state of protein expression in the lungs after radon inhalation and LPS administration and identified biomarkers that could be particularly affected. We performed shotgun proteomics and multivariate analyses and evaluated myeloperoxidase (MPO) activity. On examining the control, LPS-administration, and radon inhalation plus LPS-administered groups, the expression levels of cilia- and flagella-associated protein 61, segment polarity protein dishevelled homolog DVL-1, histone-lysine N-methyltransferase 2 A, and heat shock protein beta-1 varied and were identified as characteristic indicators. However, radon inhalation did not suppress MPO activity indicating an absence of anti-inflammatory effect in the lungs. Thus, although the combination of short-term continuous radon pre-inhalation and LPS administration cannot yet be considered effective against lung inflammation, we identified four key indicators for assessing the associated effects. Despite not clarifying the biological significance of these proteins, our findings provide useful information for applying radon therapy in systemic inflammation.