AI Article Synopsis

  • Inflammation is influenced by epigenetic modifications such as DNA methylation and histone acetylation, and the study explores how sulforaphane (SFN), an HDAC inhibitor, affects these processes during acute inflammation.
  • SFN was found to inhibit HDAC activity, promote histone acetylation, and induce DNA demethylation, leading to increased expression of immune-related genes after LPS stimulation in monocyte-derived dendritic cells.
  • The findings suggest that SFN's ability to regulate epigenetic changes may help control excessive inflammatory cytokine production, highlighting its potential as a protective and anti-inflammatory agent.

Article Abstract

Inflammation is regulated by epigenetic modifications, including DNA methylation and histone acetylation. Sulforaphane (SFN), a histone deacetylase (HDAC) inhibitor, is also a potent immunomodulatory agent, but its anti-inflammatory functions through epigenetic modifications remain unclear. Therefore, this study aimed to investigate the epigenetic effects of SFN in maintaining the immunomodulatory homeostasis of innate immunity during acute inflammation. For this purpose, SFN-induced epigenetic changes and expression levels of immune-related genes in response to lipopolysaccharide (LPS) stimulation of monocyte-derived dendritic cells (moDCs) were analyzed. These results demonstrated that SFN inhibited HDAC activity and caused histone H3 and H4 acetylation. SFN treatment also induced DNA demethylation in the promoter region of the MHC-SLA1 gene, resulting in the upregulation of Toll-like receptor 4 (TLR4), MHC-SLA1, and inflammatory cytokines' expression at 6 h of LPS stimulation. Moreover, the protein levels of cytokines in the cell culture supernatants were significantly inhibited by SFN pre-treatment followed by LPS stimulation in a time-dependent manner, suggesting that inhibition of HDAC activity and DNA methylation by SFN may restrict the excessive inflammatory cytokine availability in the extracellular environment. We postulate that SFN may exert a protective and anti-inflammatory function by epigenetically influencing signaling pathways in experimental conditions employing porcine moDCs.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8227201PMC
http://dx.doi.org/10.3390/biology10060490DOI Listing

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