Abstract

Background

Radiation exposure is known to increase the risk of chronic inflammatory diseases, such as atherosclerosis, by modulating inflammation.

Methods

To investigate the infiltration of leukocytes in radiation-aggravated atherosclerosis, we examined low-density lipoprotein receptor-deficient (Ldlr–/–) mice and C57BL/6j mice after exposure to 0.5 or 1 Gy radiation over 16 weeks.

Results

We found that radiation exposure induced atherosclerosis development in Ldlr–/– mice, as demonstrated by increased lipid-laden plaque size, reactive oxygen species levels, and levels of the pro-inflammatory cytokines, IL-1β and TNF-α, in the aortas and spleens. Total plasma cholesterol, triglyceride, and LDL cholesterol levels were also increased by radiation exposure, along with cardiovascular risk. We also showed dose-dependent increases in neutrophils and monocytes that coincided with a reduction in lymphocytes in the spleens of Ldlr–/– mice. The correlation between the infiltration of leukocytes and cytokine production was also confirmed in the hearts and spleens of these mice.

Conclusions

We concluded that chronic radiation exposure increased the production of pro-inflammatory mediators, which was associated with the migration of neutrophils and inflammatory monocytes into sites of atherosclerosis. Thus, our data suggest that the accumulation of neutrophils and inflammatory monocytes, together with the reduction of lymphocytes, contribute to aggravated atherosclerosis in Ldlr–/– mice under prolonged exposure to radiation.

中文翻译：

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慢性辐射暴露通过刺激中性粒细胞浸润而加剧动脉粥样硬化

 抽象的

 背景

众所周知，辐射暴露会通过调节炎症来增加慢性炎症性疾病的风险，例如动脉粥样硬化。

 方法

为了研究辐射加剧的动脉粥样硬化中白细胞的浸润情况，我们检查了暴露于 0.5 或 1 Gy 辐射 16 周后的低密度脂蛋白受体缺陷 (Ldlr–/–) 小鼠和 C57BL/6j 小鼠。

 结果

我们发现，辐射暴露会诱导 Ldlr–/– 小鼠出现动脉粥样硬化，这通过主动脉中脂质斑块大小、活性氧水平以及促炎细胞因子 IL-1β 和 TNF-α 水平的增加来证明。和脾脏。辐射暴露也会增加血浆总胆固醇、甘油三酯和低密度脂蛋白胆固醇水平，并增加心血管风险。我们还发现，Ldlr–/– 小鼠脾脏中的中性粒细胞和单核细胞呈剂量依赖性增加，同时淋巴细胞减少。在这些小鼠的心脏和脾脏中也证实了白细胞浸润与细胞因子产生之间的相关性。

 结论

我们得出的结论是，慢性辐射暴露增加了促炎介质的产生，这与中性粒细胞和炎性单核细胞迁移到动脉粥样硬化部位有关。因此，我们的数据表明，中性粒细胞和炎症单核细胞的积累以及淋巴细胞的减少，导致长期暴露于辐射的 Ldlr-/- 小鼠的动脉粥样硬化加重。