Exposure to PM2.5 during pregnancy causes lung inflammation in the offspring: Mechanism of action of mogrosides

Exploring the mechanism of lung injury induced by lunar dust simulant in rats based on metabolomic analysis

“…9 In addition, in experiments with pregnant mice, the mRNA levels of the inflammatory mediator Pla2g2d and its metabolites lysophosphatidylcholines (LysoPCs) and arachidonic acid (AA) were up-regulated in the lung tissue of PM2.5 group, by contrast, these inflammatory changes were recovered after treatment with mogrosides (MGs) during pregnancy; Pla2g2d was suggested to be a potential target of MGs to ameliorate PM2.5-induced lung injury. 10 These studies all confirm that metabolomic approaches are effective tools to characterize metabolic changes in air pollutioninduced lung injury. 11 Lunar dust, as the fine dust particles existing on the lunar surface, has a lung toxicity far greater than that of PM2.5 due to its special physical and chemical properties.…”

“…Volcano, column, and heat maps were constructed to visualize differences in metabolite levels for each comparison. 10 Subsequently, the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis and correlation network analysis were performed for the significantly differential metabolites.…”

“…When nuclear magnetic resonance (NMR)‐based metabolic methods were used to study the changes in the metabolic components of A549 cells treated with PM2.5, 12 metabolites were significantly changed, and the related metabolic pathways involved are similar to the results of Li et al, mainly involving amino acid metabolism, lipid metabolism, nucleotide metabolism, and the tricarboxylic acid cycle 9 . In addition, in experiments with pregnant mice, the mRNA levels of the inflammatory mediator Pla2g2d and its metabolites lysophosphatidylcholines (LysoPCs) and arachidonic acid (AA) were up‐regulated in the lung tissue of PM2.5 group, by contrast, these inflammatory changes were recovered after treatment with mogrosides (MGs) during pregnancy; Pla2g2d was suggested to be a potential target of MGs to ameliorate PM2.5‐induced lung injury 10 . These studies all confirm that metabolomic approaches are effective tools to characterize metabolic changes in air pollution‐induced lung injury 11 .…”

Advances in respiratory physiology in mouse models of experimental asthma

“…The fetal origins of adult disease hypothesis proposes that the in utero environment is critical for determining an individual’s susceptibility to certain chronic diseases later in life ( Barker, 1990 ). Notably, suboptimal nutritional status, such as undernutrition due to maternal smoking or maternal exposure to heavily polluted air, as well as toxins inhaled or ingested by pregnant mothers, play key roles in fetal underdevelopment and organ dysfunction after birth ( Wang et al, 2020 ; Chen et al, 2021 ; Li et al, 2021 ). The latent and persistent effects of fetal programming may arise from epigenetic modifications that permanently change key regulators of a range of biological processes, including cellular metabolism (e.g., mitochondrial function) and immune responses (e.g., heightened pro-inflammatory mediator production) with or without additional external environmental stimuli after birth ( Barker and Osmond, 1986 ; Petronis, 2010 ; Li et al, 2018 ; Wang et al, 2020 ; Chen et al, 2021 ).…”

“…In humans, lung morphogenesis begins at 3 to 4 weeks post-conception, followed by five stages of intense development (embryonic, pseudoglandular, canalicular, saccular, and alveolar) that occur up to 36 weeks post-conception, and completion of lung development during childhood and young adulthood. In utero environmental insults during any of the developmental stages can result in abnormal lung architecture ( Li et al, 2021 ) and function ( Harju et al, 2016 ; Lee et al, 2018 ), and increased susceptibility to asthma ( Hazlehurst et al, 2021 ) and asthma exacerbations after birth ( Gilliland et al, 2001 ). Tobacco cigarette smoke and particulate matter (PM2.5) are currently the most commonly occurring in utero toxins that impair lung function in offspring and increase their susceptibility to asthma ( Li et al, 2018 ; Wang et al, 2021b ; Chen et al, 2021 ).…”