PDF(Pubmed)
Abstract：
Airborne fine particulate matter (PM2.5) in air pollution has become a significant global public health concern related to allergic diseases. Previous research indicates that PM2.5 not only affects the respiratory system but may also induce systemic inflammation in various tissues. Moreover, its impact may vary among different populations, with potential consequences during pregnancy and in newborns. However, the precise mechanisms through which PM2.5 induces inflammatory reactions remain unclear. This study aims to explore potential pathways of inflammatory responses induced by PM2.5 through animal models and zebrafish embryo experiments. In this study, zebrafish embryo experiments were conducted to analyze the effects of PM2.5 on embryo development and survival, and mouse experimental models were employed to assess the impact of PM2.5 stimulation on various aspects of mice. Wild-type zebrafish embryos were exposed to a PM2.5 environment of 25-400 μg/mL starting at 6 h after fertilization (6 hpf). At 6 days post-fertilization, the survival rates of the 25, 50, 100, and 200 µg/mL groups were 100%, 80, 40%, and 40%, respectively. Zebrafish embryos stimulated with 25 μg/mL of PM2.5 still exhibited successful development and hatching. Additionally, zebrafish subjected to doses of 25-200 μg/mL displayed abnormalities such as spinal curvature and internal swelling after hatching, indicating a significant impact of PM2.5 stimulation on embryo development. In the mouse model, mice exposed to PM2.5 exhibited apparent respiratory overreaction, infiltration of inflammatory cells into the lungs, elevated levels of inflammatory response-related cytokines, and inflammation in various organs, including the liver, lungs, and uterus. Blood tests on experimental mice revealed increased expression of inflammatory and chemotactic cytokines, and GSEA indicated the induction of various inflammatory responses and an upregulation of the TNF-α/NFκB pathway by PM2.5. Our results provide insights into the harmful effects of PM2.5 on embryos and organs. The induced inflammatory responses by PM2.5 may be mediated through the TNF-α/NFκB pathway, leading to systemic organ inflammation. However, whether PM2.5-induced inflammatory responses in various organs and abnormal embryo development are generated through different pathways requires further study to comprehensively clarify and identify potential treatment and prevention methods.
摘要：
空气污染中的空气中的细颗粒物（PM2.5）已成为与过敏性疾病有关的重要全球公共卫生问题。先前的研究表明，PM2.5不仅影响呼吸系统，而且还可能在各种组织中引起全身性炎症。此外，它的影响可能在不同的人群中有所不同，在怀孕期间和新生儿中具有潜在的后果。然而,PM2.5诱导炎症反应的确切机制尚不清楚.本研究旨在通过动物模型和斑马鱼胚胎实验探索PM2.5诱导炎症反应的潜在途径。在这项研究中,通过斑马鱼胚胎实验,分析PM2.5对胚胎发育和存活的影响,和小鼠实验模型用于评估PM2.5刺激对小鼠各个方面的影响。从受精后6小时（6hpf）开始，将野生型斑马鱼胚胎暴露于25-400μg/mL的PM2.5环境中。受精后6天，25、50、100和200µg/mL组的存活率为100％，80,40%,40%,分别。用25μg/mLPM2.5刺激的斑马鱼胚胎仍然显示出成功的发育和孵化。此外,斑马鱼受到25-200μg/mL的剂量，在孵化后表现出异常，如脊柱弯曲和内部肿胀，表明PM2.5刺激对胚胎发育有显著影响。在老鼠模型中，暴露于PM2.5的小鼠表现出明显的呼吸过度反应，炎症细胞浸润到肺部，炎症反应相关细胞因子水平升高，和各种器官的炎症，包括肝脏,肺,还有子宫.对实验小鼠的血液测试显示炎症和趋化细胞因子的表达增加，和GSEA表明PM2.5诱导了各种炎症反应和TNF-α/NFκB途径的上调。我们的研究结果为PM2.5对胚胎和器官的有害影响提供了见解。PM2.5诱导的炎症反应可能通过TNF-α/NFκB通路介导,导致全身器官炎症。然而,PM2.5诱导的各器官炎症反应和胚胎发育异常是否通过不同的途径产生，需要进一步研究，以全面阐明和确定潜在的治疗和预防方法。
