The Interaction among Microbiota, Epigenetic Regulation, and Air Pollutants in Disease Prevention.
Alessandra PullieroDeborah TraversiElena FranchittiMartina BarchittaAlberto IzzottiAntonella AgodiPublished in: Journal of personalized medicine (2021)
Environmental pollutants can influence microbiota variety, with important implications for the general wellbeing of organisms. In subjects at high-risk of cancer, gut, and lung microbiota are distinct from those of low-risk subjects, and disease progression is associated with microbiota alterations. As with many inflammatory diseases, it is the combination of specific host and environmental factors in certain individuals that provokes disease outcomes. The microbiota metabolites influence activity of epigenetic enzymes. The knowledge of the mechanisms of action of environmental pollution now includes not only the alteration of the gut microbiota but also the interaction between different human microbiota niches such as the lung-gut axis. The epigenetic regulations can reprogram differentiated cells in response to environmental changes. The microbiota can play a major role in the progression and suppression of several epigenetic diseases. Accordingly, the maintenance of a balanced microbiota by monitoring the environmental stimuli provides a novel preventive approach for disease prevention. Metagenomics technologies can be utilized to establish new mitigation approaches for diseases induced by polluted environments. The purpose of this review is to examine the effects of particulate matter exposure on the progression of disease outcomes as related to the alterations of gut and lung microbial communities and consequent epigenetic modifications.
Keyphrases
- particulate matter
- dna methylation
- gene expression
- heavy metals
- human health
- air pollution
- endothelial cells
- healthcare
- risk assessment
- oxidative stress
- induced apoptosis
- type diabetes
- metabolic syndrome
- ms ms
- climate change
- life cycle
- cell cycle arrest
- papillary thyroid
- skeletal muscle
- young adults
- pi k akt
- endoplasmic reticulum stress