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Updated: Sep 1, 2025
Measuring Carbon Content in Airway Macrophages Exposed to Carbon-Containing Particulate Matters
Published on: July 12, 2024
Within- and cross-tissue gene regulations were disrupted by PM2.5 nitrate exposure and associated with respiratory
Jushan Zhang1, Haoxiang Cheng2, Antonio Di Narzo2
1Department of Respiratory Medicine, Shanghai Tenth People's Hospital, Tongji University, Shanghai, China; College of Environmental Science and Engineering, Tongji University, Shanghai, China.
Background:
Pathogenesis of complex diseases often involves multiple organs/tissue-types. To date, the PM2.5 exposure's toxic effects and induced disease risks were not studied at multi-tissue level.
Methods:
C57BL/6 mice (n = 40) were exposed to PM2.5 NO3- and clean air, respectively, and afterwards assessed respiratory functions and transcriptome in relevant tissues: blood and lung. We constructed within- and cross-tissue gene regulation networks and identified network modules associated with exposure and respiratory functions.
Results:
PM2.5 NO3- exposure elevated naïve B cells proportion in blood (p = 0.0028). Among the 6000 highest expressed genes in blood, 18.8 % (1133 genes) were altered by exposure at p ≤ 0.05 level, among which 763 genes were also associated with respiratory function (enrichment folds = 7.63, p = 2.7E-189). The exposure disrupted blood genes were primarily in the immunoregulation pathways. Both within- and cross-tissue gene network modules were perturbed by exposure and associated with respiratory function. An immunodeficiency related cross-tissue module of 555 genes was affected by exposure (p = 0.0023) and strongly correlated with FEV0.05/FVC (r = 0.61 and p = 3E-5).
Conclusions:
This study aims to fill in a major knowledge gap and investigated the effect of PM2.5 exposure simultaneously in multiple tissues. We provided novel evidence that PM2.5 NO3- exposure profoundly perturbed within- and cross-tissue gene regulations, and highlighted their roles in the etiology of respiratory decline.
Insights
Particulate matter (PM2.5) exposure impacts multiple tissues, affecting gene regulation and respiratory function. This study reveals PM2.5 nitrate disrupts gene networks in blood and lung, linking these changes to respiratory decline.
Area of Science:
- Environmental Health
- Toxicology
- Genomics
Background:
- Complex diseases often involve multiple organs.
- Previous studies have not comprehensively assessed the multi-tissue toxic effects of PM2.5 exposure.
Purpose of the Study:
- To investigate the simultaneous effects of PM2.5 exposure on gene regulation across multiple tissues.
- To identify gene networks perturbed by PM2.5 and their association with respiratory function decline.
Main Methods:
- Mice were exposed to PM2.5 nitrate or clean air.
- Respiratory functions and transcriptomes of blood and lung tissues were analyzed.
- Within- and cross-tissue gene regulation networks were constructed.
Main Results:
- PM2.5 nitrate exposure increased naive B cells in blood and altered gene expression.
- A significant portion of altered blood genes were linked to respiratory function and immunoregulation pathways.
- Exposure perturbed gene network modules across tissues, with one module strongly correlating with reduced FEV0.05/FVC.
Conclusions:
- PM2.5 nitrate exposure significantly disrupts gene regulation in multiple tissues.
- Cross-tissue gene network perturbations are implicated in the development of respiratory decline.
- This study provides novel insights into the multi-tissue mechanisms of PM2.5 toxicity.
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