Parental PM_2.5 exposure changes Th17/Treg cells in offspring, is associated with the elevation of blood pressure

Abstract

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/m 3 in PM chamber, whereas the average concentration in FA chamber was 9.4 ± 0.23 μg/m 3 .Similarly, during the offspring exposure, the average concentration in PM and FA chamber were 100.76 ± 26.97 μg/m 3 and 9.15 ± 0.15 μg/m 3 , 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.

The Impact of the Aryl Hydrocarbon Receptor on Antenatal Chemical Exposure-Induced Cardiovascular–Kidney–Metabolic Programming

“…The earliest AHR agonists identified were typically constituents of environmental chemicals including dioxins, BPA, phthalates, and PFOS, as well as polycyclic aromatic hydrocarbons [143]. Various chemicals have been assessed, including TCDD [117][118][119][120][121], BPA [122][123][124][125][126], DEHP [127][128][129], DBP [130,131], perfluorooctane sulfonic acid (PFOS) [132], BaP [133], Cd [134][135][136], and PM 2.5 [137,141]. Maternal exposure to the AHR ligand TCDD induces hypertension in offspring, correlated with AHR/CYP1A1 induction and TH17mediated renal inflammation [118].…”

A comprehensive understanding of ambient particulate matter and its components on the adverse health effects based from epidemiological and laboratory evidence

“…These findings demonstrated that PM 2.5 can induce inflammatory responses in which macrophages and neutrophils are involved [ 184 ]. Other studies have suggested that parental PM 2.5 could mediate Th17- and T regular-related immune microenvironment changes, leading to increased blood pressure in offspring [ 185 ]. In vitro, studies have shown that PM 2.5 may exacerbate viral myocarditis through MMP-2/TIMP-1 imbalance, perforin response and Th17-mediated viral replication [ 186 ].…”

Adverse Impact of Environmental Chemicals on Developmental Origins of Kidney Disease and Hypertension

“…Table 3 summarizes animal studies demonstrating the association between maternal environmental chemical exposure and subsequent kidney disease and hypertension in progeny ( 91 – 105 ). The current review is solely restricted to chemical exposures happening during the duration of kidney development, with a focus on reporting offspring outcomes starting after birth.…”

“…Several types of chemicals have been evaluated, including TCDD ( 88 – 90 ), BPA ( 94 , 95 ), DEHP ( 96 ), DBP ( 97 , 98 ), BaP ( 99 ), heavy metal mixture ( 100 ), Cd ( 101 – 103 ), and PM 2.5 ( 104 , 105 ). Maternal exposure to TCDD or BPA causes the rise of BP in adult rat offspring ( 91 , 92 , 94 ), which was relevant to dysregulated AHR signaling pathway.…”

“…Additionally, prenatally Cd-exposed offspring rats presented the features of kidney injury in other three studies ( 101 – 103 ), while no prior studies have addressed the effects of Pb or Hg. Furthermore, air pollution was shown to lead to hypertension in rats or mice prenatally exposed to PM 2.5 ( 104 , 105 ).…”