Epigenetic Mechanisms in Inflammation

Bayarsaihan, Dashzeveg

doi:10.1177/0022034510378683

Cited by 232 publications

(197 citation statements)

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“…42,43 Finally, as these processes may be perpetuated through inflammatory pathways, the role of chronic inflammation and its modification through anti-inflammatory medications (either intended or pleiotropic) is another potential target of future research in the area. 44 We used microarrays as a cost-effective approach to interrogate epigenome-wide DNA methylation changes associated with THM exposure. However, there are several analytical gaps in the Infinium HumanMethylation450 BeadChip analyses, as there is no consensus for preprocessing and downstream analysis of the data.…”

Section: Discussionmentioning

confidence: 99%

DNA methylation levels and long-term trihalomethane exposure in drinking water: an epigenome-wide association study

et al. 2015

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Trihalomethanes (THM) are undesired disinfection byproducts (DBPs) formed during water treatment. Mice exposed to DBPs showed global DNA hypomethylation and c-myc and c-jun gene-specific hypomethylation, while evidence of epigenetic effects in humans is scarce. We explored the association between lifetime THM exposure and DNA methylation through an epigenome-wide association study. We selected 138 population-based controls from a casecontrol study of colorectal cancer conducted in Barcelona, Spain, exposed to average lifetime THM levels 85 mg/L vs. >85 mg/L (N D 68 and N D 70, respectively). Mean age of participants was 70 years, and 54% were male. Average lifetime THM level in the exposure groups was 64 and 130 mg/L, respectively. DNA was extracted from whole blood and was bisulphite converted to measure DNA methylation levels using the Illumina HumanMethylation450 BeadChip. Data preprocessing was performed using RnBeads. Methylation was compared between exposure groups using empirical Bayes moderated linear regression for CpG sites and Gaussian kernel for CpG regions. ConsensusPathDB was used for gene set enrichment. Statistically significant differences in methylation between exposure groups was found in 140 CpG sites and 30 gene-related regions, after false discovery rate <0.05 and adjustment for age, sex, methylation first principal component, and blood cell proportion. The annotated genes were localized to several cancer pathways. Among them, 29 CpGs had methylation levels associated with THM levels (|Db| 0.05) located in 11 genes associated with cancer in other studies. Our results suggest that THM exposure may affect DNA methylation in genes related to tumors, including colorectal and bladder cancers. Future confirmation studies are required.

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Section: Discussionmentioning

confidence: 99%

DNA methylation levels and long-term trihalomethane exposure in drinking water: an epigenome-wide association study

et al. 2015

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“…Establishment of the chronic inflammatory state is determined not only by genetic factors, but also by environmental factors through epigenetic modifications (Bayarsaihan 2011). DNA methylation, the covalent addition of methyl groups to the cytosine base of CpG dinucleotide, is one of the most studied epigenetic modifications.…”

Section: Introductionmentioning

confidence: 99%

Transcriptomic and epigenetic analyses reveal a gender difference in aging-associated inflammation: the Vitality 90+ study

Nevalainen

Kananen

Marttila

et al. 2015

AGE

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Aging is associated with a pro-inflammatory state, often referred to as inflammaging. The origin of the pro-inflammatory mediators and their role in the pathogenesis of the aging-associated diseases remain poorly understood. As aging is also associated with profound changes in the transcriptomic and epigenetic (e.g., DNA methylation) profiles of cells in the peripheral blood, we analyzed the correlation of these profiles with inflammaging using the Bclassical^marker interleukin-6 as an indicator. The analysis of the whole-genome peripheral blood mononuclear cell (PBMC) gene expression revealed 62 transcripts with expression levels that significantly correlated with the plasma interleukin-6 (IL-6) levels in men, whereas no correlations were observed in women. The Gene Ontology analysis of plasma IL-6-associated transcripts in men revealed processes that were linked to the inflammatory response. Additionally, an Ingenuity Pathway Analysis (IPA) pathway analysis identified Tec kinase signaling as an affected pathway and upstream regulator analysis predicted the activation of IL-10 transcript. D N A m e t h y l a t i o n w a s a s s e s s e d u s i n g a HumanMethylation450 array. Seven genes with expression profiles that were associated with the plasma IL-6 levels in men were found to harbor CpG sites with methylation levels that were also associated with the IL-6 levels. Among these genes were IL1RN, CREB5, and FAIM3, which mapped to a network of inflammatory response genes. According to our results, inflammaging is manifested differently at the genomic level in nonagenarian men and women. Part of this difference seems to be of epigenetic origin. These AGE (2015) 37:76 DOI 10.1007 Electronic supplementary material The online version of this article (doi:10.1007/s11357-015-9814-9) contains supplementary material, which is available to authorized users. differences point to the genomic regulation of inflammatory response and suggest that the gender-specific immune system dimorphism in older individuals could be accounted for, in part, by DNA methylation.

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“…Dayarsaihan [7] stated that progress in research of epigenetics in inflammatory response opens opportunities for the development of efficient medications for particular therapies. Some of the drugs proposed for the therapy are histone deacetylase inhibitors and de-methylating agents.…”

Section: Journal Of Clinical Epigenetics Issn 2472-1158mentioning

confidence: 99%