Epigenetic Control of Macrophage Polarisation and Soluble Mediator Gene Expression during Inflammation

Research output: Contribution to journalReview article

Authors

Colleges, School and Institutes

External organisations

  • Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK.

Abstract

Macrophages function as sentinel cells, which constantly monitor the host environment for infection or injury. Macrophages have been shown to exhibit a spectrum of activated phenotypes, which can often be categorised under the M1/M2 paradigm. M1 macrophages secrete proinflammatory cytokines and chemokines, such as TNF-α, IL-6, IL-12, CCL4, and CXCL10, and induce phagocytosis and oxidative dependent killing mechanisms. In contrast, M2 macrophages support wound healing and resolution of inflammation. In the past decade, interest has grown in understanding the mechanisms involved in regulating macrophage activation. In particular, epigenetic control of M1 or M2 activation states has been shown to rely on posttranslational modifications of histone proteins adjacent to inflammatory-related genes. Changes in methylation and acetylation of histones by methyltransferases, demethylases, acetyltransferases, and deacetylases can all impact how macrophage phenotypes are generated. In this review, we summarise the latest advances in the field of epigenetic regulation of macrophage polarisation to M1 or M2 states, with particular focus on the cytokine and chemokine profiles associated with these phenotypes.

Details

Original languageEnglish
Pages (from-to)6591703
JournalMediators of Inflammation
Volume2016
Publication statusPublished - 2016

Keywords

  • Animals, Chemokine CCL4, Chemokine CXCL10, Epigenesis, Genetic, Humans, Inflammation, Interleukin-12, Interleukin-6, Macrophage Activation, Macrophages, Tumor Necrosis Factor-alpha, Journal Article, Research Support, Non-U.S. Gov't, Review