Epidemiological evidences have indicated that fine particulate matter (PM_2.5) exposure is associated with the occurrence and development of hypertension. The present study aims to explore the effects of parental PM_2.5 exposure on blood pressure in offspring and elucidate the potential mechanism. The parental male and female C57BL/6 mice were exposed to concentrated PM_2.5 or filtered air (FA) using Shanghai Meteorological and Environmental Animal Exposure System (Shanghai‐METAS) for 16 weeks. At week 12, the mice were assigned to breed offspring. The male offspring mice were further exposed to PM_2.5 or FA as above method. During the parental exposure, the average PM_2.5 concentration was 133.7 ± 53.32 μg/m³ in PM chamber, whereas the average concentration in FA chamber was 9.4 ± 0.23 μg/m³. Similarly, during the offspring exposure, the average concentration in PM and FA chamber were 100.76 ± 26.97 μg/m³ and 9.15 ± 0.15 μg/m³, respectively. The PM_2.5‐exposed offspring mice displayed the elevation of blood pressure, the increase of angiotensin II (Ang II), the decrease of angiotensin converting enzyme 2 (ACE2) and Ang (1–7) in serum when compared with the FA‐exposed offspring mice. The similar results displayed in the proteins expression of ACE2, AT1R, and Ang (1–7) in vessel and kidney. More importantly, parental PM exposure further induced the increase in serous Ang II and the protein expression of AT1R in vessel, but decrease in ACE2 and Ang (1–7). The serous Ang II was positively associated with splenic T helper type 17 (Th17) cell population and serous IL (interleukin)‐17A, but negatively associated with T regular (Treg) cell population and serous IL‐10. The results suggested that parental air pollution exposure might induce the elevation of offspring blood pressure via mediate Th17‐ and Treg‐related immune microenvironment.

中文翻译：

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父母的PM2.5暴露会改变后代的Th17 / Treg细胞，与血压升高有关

流行病学证据表明，细颗粒物（PM _2.5）暴露与高血压的发生和发展有关。本研究旨在探讨父母暴露PM _2.5对后代血压的影响并阐明其潜在机制。使用上海气象和环境动物暴露系统（Shanghai-METAS）将雄性和雌性C57BL / 6雌性和雌性小鼠暴露于浓缩的PM _2.5或过滤空气（FA）中16周。在第12周，将小鼠分配为繁殖后代。按照上述方法，将雄性后代小鼠进一步暴露于PM _2.5或FA。在父母暴露期间，PM _2.5的平均浓度为133.7±53.32μg/ mPM室中的平均浓度为³，而FA室中的平均浓度为9.4±0.23μg/ m ³。同样，在后代暴露期间，PM和FA腔室中的平均浓度分别为100.76±26.97μg/ m ³和9.15±0.15μg/ m ³。PM _2.5与暴露于FA的后代小鼠相比，暴露后代的小鼠表现出血压升高，血管紧张素II（Ang II）升高，血清血管紧张素转化酶2（ACE2）和Ang（1–7）降低。在血管和肾脏中ACE2，AT1R和Ang（1-7）的蛋白质表达中也显示出相似的结果。更重要的是，父母PM暴露进一步诱导了浆液性Ang II的增加和血管中AT1R的蛋白表达，但ACE2和Ang降低（1–7）。浆液性Ang II与脾T辅助型17（Th17）细胞群和浆液性IL（白介素）-17A呈正相关，而与T常规（Treg）细胞群体和浆液性IL-10呈负相关。