tetano
Editor, Senior Moderator
Sci Rep
. 2023 Nov 7;13(1):19259.
doi: 10.1038/s41598-023-46724-6. Transcriptomics profile of human bronchial epithelial cells exposed to ambient fine particles and influenza virus (H3N2)
Yuan Liu[SUP] 1 [/SUP], Yinbiao Wang[SUP] 1 [/SUP], Rui Zhang[SUP] 1 [/SUP], Shaolan Wang[SUP] 1 [/SUP], Juan Li[SUP] 1 [/SUP], Zhen An[SUP] 1 [/SUP], Jie Song[SUP] 1 [/SUP], Weidong Wu[SUP] 2 [/SUP]
Affiliations
Fine particulate matter (PM[SUB]2.5[/SUB]) pollution remains a major threat to public health. As the physical barrier against inhaled air pollutants, airway epithelium is a primary target for PM[SUB]2.5[/SUB] and influenza viruses, two major environmental insults. Recent studies have shown that PM[SUB]2.5[/SUB] and influenza viruses may interact to aggravate airway inflammation, an essential event in the pathogenesis of diverse pulmonary diseases. Airway epithelium plays a critical role in lung health and disorders. Thus far, the mechanisms for the interactive effect of PM[SUB]2.5[/SUB] and the influenza virus on gene transcription of airway epithelial cells have not been fully uncovered. In this present pilot study, the transcriptome sequencing approach was introduced to identify responsive genes following individual and co-exposure to PM[SUB]2.5[/SUB] and influenza A (H3N2) viruses in a human bronchial epithelial cell line (BEAS-2B). Enrichment analysis revealed the function of differentially expressed genes (DEGs). Specifically, the DEGs enriched in the xenobiotic metabolism by the cytochrome P450 pathway were linked to PM[SUB]2.5[/SUB] exposure. In contrast, the DEGs enriched in environmental information processing and human diseases, such as viral protein interaction with cytokines and cytokine receptors and epithelial cell signaling in bacterial infection, were significantly related to H3N2 exposure. Meanwhile, co-exposure to PM[SUB]2.5[/SUB] and H3N2 affected G protein-coupled receptors on the cell surface. Thus, the results from this study provides insights into PM[SUB]2.5[/SUB]- and influenza virus-induced airway inflammation and potential mechanisms.
. 2023 Nov 7;13(1):19259.
doi: 10.1038/s41598-023-46724-6. Transcriptomics profile of human bronchial epithelial cells exposed to ambient fine particles and influenza virus (H3N2)
Yuan Liu[SUP] 1 [/SUP], Yinbiao Wang[SUP] 1 [/SUP], Rui Zhang[SUP] 1 [/SUP], Shaolan Wang[SUP] 1 [/SUP], Juan Li[SUP] 1 [/SUP], Zhen An[SUP] 1 [/SUP], Jie Song[SUP] 1 [/SUP], Weidong Wu[SUP] 2 [/SUP]
Affiliations
- PMID: 37935887
- PMCID: PMC10630401
- DOI: 10.1038/s41598-023-46724-6
Fine particulate matter (PM[SUB]2.5[/SUB]) pollution remains a major threat to public health. As the physical barrier against inhaled air pollutants, airway epithelium is a primary target for PM[SUB]2.5[/SUB] and influenza viruses, two major environmental insults. Recent studies have shown that PM[SUB]2.5[/SUB] and influenza viruses may interact to aggravate airway inflammation, an essential event in the pathogenesis of diverse pulmonary diseases. Airway epithelium plays a critical role in lung health and disorders. Thus far, the mechanisms for the interactive effect of PM[SUB]2.5[/SUB] and the influenza virus on gene transcription of airway epithelial cells have not been fully uncovered. In this present pilot study, the transcriptome sequencing approach was introduced to identify responsive genes following individual and co-exposure to PM[SUB]2.5[/SUB] and influenza A (H3N2) viruses in a human bronchial epithelial cell line (BEAS-2B). Enrichment analysis revealed the function of differentially expressed genes (DEGs). Specifically, the DEGs enriched in the xenobiotic metabolism by the cytochrome P450 pathway were linked to PM[SUB]2.5[/SUB] exposure. In contrast, the DEGs enriched in environmental information processing and human diseases, such as viral protein interaction with cytokines and cytokine receptors and epithelial cell signaling in bacterial infection, were significantly related to H3N2 exposure. Meanwhile, co-exposure to PM[SUB]2.5[/SUB] and H3N2 affected G protein-coupled receptors on the cell surface. Thus, the results from this study provides insights into PM[SUB]2.5[/SUB]- and influenza virus-induced airway inflammation and potential mechanisms.