Abstract
Background
Exposure to particulate matter (PM) and house dust mite (HDM) can change the expression patterns of inflammation-, oxidative stress-, and cell death-related genes. We investigated the changes in gene expression patterns owing to PM exposure.
Objective
This study examined the changes in gene expression patterns following PM exposure.
Methods
We searched for differentially expressed genes (DEGs) following PM exposure using five cell line-based RNA-seq or microarray datasets and six human-derived datasets. The enrichment terms of the DEGs were assessed.
Results
DEG analysis yielded two gene sets. Thus, enrichment analysis was performed for each gene set, and the enrichment terms related to respiratory diseases were presented. The intersection of six human-derived datasets and two gene sets was obtained, and the expression patterns following PM exposure were observed.
Conclusions
Two gene sets were obtained for cells treated with PM and their expression patterns were presented following verification in human-derived cells. Our findings suggest that exposure to PM2.5 and HDM may reveal changes in genes that are associated with diseases, such as allergies, highlighting the importance of mitigating PM2.5 and HDM exposure for disease prevention.
Highlights
Two gene sets with differences in expression were obtained after the treatment of cells with PM.
Enrichment terms for each gene set were extracted.
DEGs in patient-derived cells after PM treatment were compared with those in cell lines.
When PBMC-derived cells were treated with PM, a relatively high overlap of DEGs was found.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
References
Abbas I et al (2019) In vitro evaluation of organic extractable matter from ambient PM2.5 using human bronchial epithelial BEAS-2B cells: cytotoxicity, oxidative stress, pro-inflammatory response, genotoxicity, and cell cycle deregulation. Environ Res 171:510–522. https://doi.org/10.1016/j.envres.2019.01.052
Barrett T et al (2012) NCBI GEO: archive for functional genomics data sets—update. Nucleic Acids Res 41:D991–D995
Chu J-H, Hart JE, Chhabra D, Garshick E, Raby BA, Laden F (2016) Gene expression network analyses in response to air pollution exposures in the trucking industry. Environ Health 15:101. https://doi.org/10.1186/s12940-016-0187-z
Guo C, Lv S, Liu Y, Li Y (2022) Biomarkers for the adverse effects on respiratory system health associated with atmospheric particulate matter exposure. J Hazard Mater 421:126760. https://doi.org/10.1016/j.jhazmat.2021.126760
Huang SK et al (2021) Effect of concentration and duration of particulate matter exposure on the transcriptome and DNA methylome of bronchial epithelial cells. Environ Epigenetics 7:dvaa022. https://doi.org/10.1093/eep/dvaa022
Kim DI, Song M-K, Kim H-I, Han KM, Lee K (2020) Diesel Exhaust particulates Induce Neutrophilic Lung inflammation by modulating endoplasmic reticulum stress-mediated CXCL1/KC expression in alveolar macrophages. Molecules 25. https://doi.org/10.3390/molecules25246046
Lee Y-G, Lee P-H, Choi S-M, An M-H, Jang A-S (2021) Effects of Air pollutants on Airway diseases. Int J Environ Res Public Health 18. https://doi.org/10.3390/ijerph18189905
Liu W-C, Chiu H-W, Chou C-L, Chiu Y-J, Lee Y-H (2023) Lactoferrin attenuated urban particulate matter-induced nephrotoxicity by regulating the CSF2/CENPE axis. Environ Pollut 318:120871. https://doi.org/10.1016/j.envpol.2022.120871
Mazzoli-Rocha F, Fernandes S, Einicker-Lamas M, Zin WA (2010) Roles of oxidative stress in signaling and inflammation induced by particulate matter. Cell Biol Toxicol 26:481–498
Misiukiewicz-Stępien P et al (2022) RNA-Seq analysis of UPM-Exposed epithelium co-cultivated with macrophages and dendritic cells in Obstructive Lung diseases. Int J Mol Sci 23. https://doi.org/10.3390/ijms23169125
Montgomery MT et al (2020) Genome-wide analysis reveals Mucociliary Remodeling of the nasal Airway Epithelium Induced by Urban PM(2.5). Am J Respiratory Cell Mol Biology 63:172–184. https://doi.org/10.1165/rcmb.2019-0454OC
Park E-J et al (2017) Ambient fine particulate matters induce cell death and inflammatory response by influencing mitochondria function in human corneal epithelial cells. Environ Res 159:595–605
Peretz A et al (2007) Diesel Exhaust Inhalation and Assessment of Peripheral Blood mononuclear cell gene transcription effects: an exploratory study of healthy human volunteers. Inhalation Toxicol 19:1107–1119. https://doi.org/10.1080/08958370701665384
Rao X, Zhong J, Brook RD, Rajagopalan S (2018) Effect of particulate matter air pollution on cardiovascular oxidative stress pathways. Antioxid Redox Signal 28:797–818
Risom L, Møller P, Loft S (2005) Oxidative stress-induced DNA damage by particulate air pollution. Mutat Research/Fundamental Mol Mech Mutagen 592:119–137
Romani A et al (2018) Keratinocytes oxidative damage mechanisms related to airborne particle matter exposure. Mech Ageing Dev 172:86–95
Ru Q et al (2017) Lipopolysaccharide accelerates fine particulate matter-induced cell apoptosis in human lung bronchial epithelial cells. Int J Occup Med Environ Health 31:173–183
Sukuman T, Ueda K, Sujaritpong S, Praekunatham H, Punnasiri K, Wimuktayon T, Prapaspongsa T (2023) Health impacts from PM2. 5 Exposure Using Environmental Epidemiology and Health Risk Assessment: a review. Appl Environ Res 45
Sung Y-Y et al (2023) Siraitia Grosvenorii Extract attenuates airway inflammation in a mouse model of respiratory Disease Induced by Particulate Matter 10 plus Diesel Exhaust particles. Nutrients 15. https://doi.org/10.3390/nu15194140
Troy NM, Hollams EM, Holt PG, Bosco A (2016) Differential gene network analysis for the identification of asthma-associated therapeutic targets in allergen-specific T-helper memory responses. BMC Med Genom 9:9. https://doi.org/10.1186/s12920-016-0171-z
van Eeden SF et al (2001) Cytokines involved in the systemic inflammatory response induced by exposure to particulate matter air pollutants (PM10). Am J Respir Crit Care Med 164:826–830
Wu J et al (2017) Fine particle matters induce DNA damage and G2/M cell cycle arrest in human bronchial epithelial BEAS-2B cells. Environ Sci Pollut Res 24:25071–25081
Xu F et al (2020) Investigation of the chemical components of ambient fine particulate matter (PM2. 5) associated with in vitro cellular responses to oxidative stress and inflammation. Environ Int 136:105475
Ye Q, Zhang T, Mao JH (2020) Haze facilitates sensitization to house dust mites in children. Environ Geochem Health 42:2195–2203. https://doi.org/10.1007/s10653-019-00481-6
Yuan C-S, Lai C-S, Tseng Y-L, Hsu P-C, Lin C-M, Cheng F-J (2021) Repeated exposure to fine particulate matter constituents lead to liver inflammation and proliferative response in mice. Ecotoxicol Environ Saf 224:112636
Zhang S et al (2023) Mutagenicity of PM2.5 and ethnic susceptibility in Chengdu-Chongqing Economic Circle, China. Sci Total Environ 879:163022. https://doi.org/10.1016/j.scitotenv.2023.163022
Funding
This work was supported by the Korea Environmental Industry & Technology Institute (KEITI), funded by the Korea Ministry of Environment (MOE) (1485019161, RS-2022-KE-002339).
Author information
Authors and Affiliations
Corresponding authors
Additional information
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
Electronic supplementary material
Below is the link to the electronic supplementary material.
Rights and permissions
Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.
About this article
Cite this article
Roh, S., Hwang, J., Park, JH. et al. Particulate matter-induced gene expression patterns in human-derived cells based on 11 public gene expression datasets. Genes Genom (2024). https://doi.org/10.1007/s13258-024-01512-y
Received:
Accepted:
Published:
DOI: https://doi.org/10.1007/s13258-024-01512-y