Gene Expression Changes Induced by Exposure of RAW 264.7 Macrophages to Particulate Matter of Air Pollution: The Role of Endotoxins.
Adam RomanMichal KorostynskiMonika Jankowska-KieltykaMarcin PiechotaJacek HajtoIrena NalepaPublished in: Biomolecules (2022)
Despite the variable chemical and physical characteristics of particulate air pollutants, inflammation and oxidative stress have been identified as common mechanisms for cell damage and negative health influences. These effects are produced by organic components, especially by endotoxins. This study analyzed the gene expression profile after exposure of RAW 264.7 cells to the standard particulate matter (PM) material, NIST1648a, and PM with a reduced organic matter content, LAp120, in comparison to the effects of lipopolysaccharide (LPS). The selected parameters of cell viability, cell cycle progression, and metabolic and inflammatory activity were also investigated. Both forms of PM negatively influenced the parameters of cell activity. These results were generally reflected in the gene expression profile. Only NIST1648a, excluding LAp120, contained endotoxins and showed small but statistically significant pro-inflammatory activity. However, the gene expression profiling revealed strong pro-inflammatory cell activation induced by NIST1648a that was close to the effects of LPS. Changes in gene expression triggered by LAp120 were relatively small. The observed differences in the effects of NIST1648a and LAp120 were related to the content of organic matter in which bacterial endotoxins play an important role. However, other organic compounds and their interactions with other PM components also appear to be of significant importance.
Keyphrases
- particulate matter
- air pollution
- oxidative stress
- gene expression
- organic matter
- cell cycle
- single cell
- genome wide
- inflammatory response
- induced apoptosis
- dna methylation
- cell therapy
- lung function
- copy number
- genome wide identification
- public health
- cell proliferation
- immune response
- cell cycle arrest
- mesenchymal stem cells
- dna damage
- risk assessment
- chronic obstructive pulmonary disease
- cystic fibrosis
- water soluble
- ischemia reperfusion injury
- endoplasmic reticulum stress
- anti inflammatory
- signaling pathway
- climate change
- social media
- human health
- atomic force microscopy
- heat stress
- heat shock