While radiation-induced lung injury (RILI) is known to be progressed by Th2 skewed, pro-inflammatory immune response, there have been few therapeutic attempts through Th1 immune modulation. We investigated whether the immunostimulant CpG-oligodeoxynucleotide (CpG-ODN) would be effective against RILI by way of measuring reactive oxygen species (ROS) and nitric oxides (NO), histopathology, micro-three-dimensional computer tomography (CT), and cytokine profiling. We found that KSK CpG-ODN (K-CpG) significantly reduced histopathological fibrosis when compared to the positive control (PC) group (p < 0.01). The levels of ROS production in serum and splenocyte of PC group were significantly higher than that of K-CpG group (p < 0.01). The production of nitric oxide (NO) in CpG-ODNs group was higher than that of PC group. Last, cytokine profiling illustrated that the protein concentrations of Th1-type cytokines such as IL-12 and TNF-α as well as Th2-type cytokine IL-5 in K-CpG group inclined to be significantly (p < 0.001 or p < 0.01) higher than those of in PC group. Collectively, our study clearly indicates that K-CpG is effective against RILI in mice by modulating the innate immune response. To our knowledge, this is the first note on anti-RILI effect of human type, K-CpG, clinically implying the potential of immunotherapy for RILI control.

虽然已知辐射诱导的肺损伤（RILI）通过Th2偏向的促炎性免疫反应而进展，但很少有通过Th1免疫调节的治疗尝试。我们通过测量活性氧（ROS）和一氧化氮（NO），组织病理学，微型三维计算机断层扫描（CT）和细胞因子来研究免疫刺激性CpG-寡脱氧核苷酸（CpG-ODN）是否对RILI有效分析。我们发现，与阳性对照组（PC）组相比，KSK CpG-ODN（K-CpG）显着减少了组织病理学纤维化（p  <0.01）。PC组血清和脾细胞ROS产生水平明显高于K-CpG组（p <0.01）。CpG-ODNs组的一氧化氮（NO）产量高于PC组。最后，细胞因子谱分析表明，K-CpG组的Th1型细胞因子如IL-12和TNF-α以及Th2型细胞因子IL-5的蛋白质​​浓度倾向于显着（p  <0.001或p  <0.01 ）高于PC组中的。总体而言，我们的研究清楚地表明，K-CpG可通过调节先天免疫应答来有效抵抗RILI。就我们所知，这是关于人类型K-CpG的抗RILI效应的首次记录，临床上暗示了免疫疗法对RILI控制的潜力。