Radiation therapy is widely used for thoracic cancers. However, it occasionally causes radiationinduced lung injuries, including pneumonitis and fibrosis. Chung-Sang-Bo-Ha-Tang (CSBHT) has been traditionally used to treat chronic pulmonary disease in Korea. PM014, a modified herbal formula derived from CSBHT, contains medicinal herbs of seven species. In our previous studies, PM014 exhibited anti-inflammatory effects in a chronic obstructive pulmonary disease model. In this study, we have evaluated the effects of PM014 on radiation-induced lung inflammation. Mice in the treatment group were orally administered PM014 six times for 2 weeks. Effects of PM014 on radiation pneumonitis were evaluated based on histological findings and differential cell count in bronchoalveolar lavage fluid. PM014 treatment significantly inhibited immune cell recruitment and collagen deposition in lung tissue. Normal lung volume, evaluated by radiological analysis, in PM014-treated mice was higher compared to that in irradiated control mice. PM014-treated mice exhibited significant changes in inspiratory capacity, compliance and tissue damping and elastance. Additionally, PM014 treatment resulted in the downregulation of inflammatory cytokines, chemokines, and fibrosis-related genes and a reduction in the transforming growth factor-β1-positive cell population in lung tissue. Thus, PM014 is a potent therapeutic agent for radiation-induced lung fibrosis and inflammation.

Forkhead transcription factor 3 (Foxp3) has a critical role in regulatory T cells (Treg). There are an increasing number of researches concerning the functions of Foxp3 in other cells, including lung epithelial cells besides Treg. However, the roles of Foxp3 in lung epithelial cells remain poorly understood. To examine the potential therapeutic benefits of Foxp3 for lung inflammation, this study investigates the effect of adenovirus-mediated Foxp3 overexpression in a radiation-induced lung damage model. Foxp3-EGFP expressing adenovirus was administered by intratracheal injection three times over 14 days after focal X-ray irradiation. To evaluate effects of Foxp3 overexpression in radiation-induced lung inflammation, immune cell profiles of bronchoalveolar lavage (BAL) fluid were analyzed. Foxp3 gene-delivered mice showed significant inhibition of immune cell infiltration, such as eosinophils, lymphocytes, macrophages and neutrophils in BAL fluid. Histopathological analysis also showed that Foxp3 overexpression inhibits inflammatory cell recruitment and collagen deposition in lung tissues. In addition, expression of inflammatory and fibrosis-related genes was decreased in the Foxp3 expression adenovirus-infected group. These results suggest that Foxp3 expression in lungs holds considerable therapeutic potential for attenuating inflammation and fibrosis in radiation-induced lung injury.

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system that leads to substantial disability through deficits of sensation and of motor, autonomic, and neuro-cognitive function. Many clinical and pathological features of experimental autoimmune encephalomyelitis (EAE) show close similarity to MS. Bee venom (BV) has been used in the practice of oriental medicine and evidence from the literature indicates that BV plays an anti-inflammatory or anti-nociceptive role against inflammatory reactions associated with arthritis and other inflammatory diseases. The purpose of the present study was to determine whether BV could suppress immune cell differentiation and infiltration into spinal cord on EAE mice commonly used as a model for MS. BV treatment increased the population of CD4+CD25+Foxp3+ T cells and inhibited CD4+ T-cell proliferation in vitro. In vivo, BV treatment increased the population of CD4+CD25+Foxp3+ T cells. Furthermore, BV administration reduced the severity of EAE while concurrently decreasing INF-y producing CD4+ T cells, IL-17A producing CD4+ T cells and inflammatory cytokine production including INF-y, IL-17A, TNF and IL-6. BV-treated animals exhibited less infiltration and preserved morphology compared to saline-treated animals. Interestingly, the therapeutic effects of BV on EAE disappeared when CD4+CD25+Foxp3+ T cells were depleted by using anti-CD25 antibody. Our research suggests that BV could be a potential therapeutic agent for antiinflammatory effects in an animal model of EAE.Multiple sclerosis (MS) is a chronic inflammatory disease ofthe central nervous system that afflicts more than one million people worldwide (1). MS leads to substantial disability through deficits of sensation and of motor, autonomic, and neuro-cognitive function (2). The pathogenesis of MS is generally considered to be an autoimmune pathology in which show close similarity to MS; therefore, EAE has commonly been used as an animal model system to study the pathogenetic mechanism of MS and test the efficacy of potential therapeutic agents for MS (6). Disease-modifying treatments such as IFN-P and glatiramer acetate have been widely applied for the treatment of MS over the last decade and have shown a beneficial effect. However, because of the limitations of conventional therapy, many patients with MS explore alternative treatment options (7). It is noteworthy that 50-75% ofMS patients use one or more complementary and alternative medicinal

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