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Metabolic and Innate Immune Memory Alterations in Human Monocytes on Chiang-Mai-PM2.5 Stimulation

ABSTRACT: The rise of PM2.5 in air pollution correlates with increased disease exacerbation, especially in asthma. This study aims to examine how Chiang-Mai, Thailand PM2.5 (CM-PM2.5) affects innate immune responses in primary human monocytes. A transcriptomic profile was obtained from cells that were stimulated with low and high doses of CM-PM2.5 (5 and 20 μg/ml) for 24 hr. The data indicated that primary human monocytes respond to CM-PM2.5 in a dose-dependent manner. The pyrimidine ribonucleotide metabolism was predominant in both datasets, but the suppression of glycolytic rate was found in high doses of CM-PM2.5 stimulation. The upregulation of the key metabolic genes was unable to compensate for the suppression. Moreover, CM-PM2.5 priming induced immune tolerance during subsequent LPS stimulation in primary human monocytes from asthma.

ORGANISM(S): Homo sapiens

PROVIDER: GSE237963 | GEO | 2026/06/02

REPOSITORIES: GEO

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Project description:Atmospheric fine particulate matter (PM2.5) causes severe haze in China and is regarded as a threat to human health. The health effects of PM2.5 vary location by location due to the variation in size distribution, chemical com position, and sources. In this study, the cytotoxicity effect, oxidative stress, and gene expression regulation of PM2.5 in Chengdu and Chongqing, two typical urban areas in southern China, were evaluated. Urban PM2.5 in summer and winter significantly inhibited cell viability and increased reactive oxygen species (ROS) levels in A549 cells. Notably, PM2.5 in winter exhibited higher cytotoxicity and ROS level than summer. Moreover, in this study, PM2.5 commonly induced cancer-related gene expression such as cell adhesion molecule 1(PECAM1), interleukin 24 (IL24), and cytochrome P450 (CYP1A1); meanwhile, PM2.5 commonly acted on cancer-related biological functions such as cell-substrate junction, cell-cell junction, and focal adhesion. In partic ular, PM2.5 in Chengdu in summer had the highest carcinogenic potential among PM2.5 at the two sites in summer and winter. Importantly, cancer-related genes were uniquely targeted by PM2.5, such as epithelial splicing regu latory protein 1 (ESRP1) and membrane-associated ring-CH-type finger 1 (1-Mar) by Chengdu summer PM2.5; collagen type IX alpha 3 chain (COL9A3) by Chengdu winter PM2.5; SH2 domain-containing 1B (SH2D1B) by Chongqing summer PM2.5; and interleukin 1 receptor-like 1 (IL1RL1) and zinc finger protein 42 (ZNF423) by Chongqing winter PM2.5. Meanwhile, important cancer-related biological functions were specially induced by PM2.5, such as cell cycle checkpoint by Chengdu summer PM2.5; macromolecule methylation by Chengdu win ter PM2.5; endoplasmic reticulum-Golgi intermediate compartment membrane by Chongqing summer PM2.5;and cellular lipid catabolic process by Chongqing winter PM2.5. Conclusively, in the typical urban areas of southern China, both summer and winter PM2.5 illustrated significant gene regulation effects. This study contrib utes to evaluating the adverse health effects of PM2.5 in southern China and providing public health suggestions for policymakers.

Dataset Information

Metabolic and Innate Immune Memory Alterations in Human Monocytes on Chiang-Mai-PM2.5 Stimulation

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