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We performed a multi-ethnic Epigenome Wide Association study on 22,774 individuals to describe the DNA methylation signature of chronic low-grade inflammation as measured by C-Reactive protein (CRP). We find 1,511 independent differentially methylated loci associated with CRP. These CpG sites show correlation structures across chromosomes, and are primarily situated in euchromatin, depleted in CpG islands. These genomic loci are predominantly situated in transcription factor binding sites and genomic enhancer regions. Mendelian randomization analysis suggests altered CpG methylation is a consequence of increased blood CRP levels. Mediation analysis reveals obesity and smoking as important underlying driving factors for changed CpG methylation. Finally, we find that an activated CpG signature significantly increases the risk for cardiometabolic diseases and COPD.

Original publication

DOI

10.1038/s41467-022-29792-6

Type

Journal article

Journal

Nature communications

Publication Date

05/2022

Volume

13

Addresses

Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK. matthias.wielscher@meduniwien.ac.at.

Keywords

BIOS consortium, Humans, Inflammation, C-Reactive Protein, DNA Methylation, CpG Islands, Nucleotide Motifs