Abstract
Previously, we reported that microglial expression of histone deacetylases 1 and 2 (Hdac1 and Hdac2) is required for microglial maturation and modulates disease progression in a mouse model of Alzheimer’s disease. Here, we analyze the role of microglial expression of Hdac1 and Hdac2 in another disease paradigm, namely experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis. The aim of this study was to ascertain whether microglial expression of these two epigenetic regulators modulates disease progression in the context of autoimmune disease. Hdac1 and Hdac2 were knocked out either individually or in combination using a microglia-specific, tamoxifen-inducible Cre-deleter line (Cx3cr1-CreERT2). The clinical course as well as histopathological changes during EAE were assessed in adult mice lacking microglial expression of these genes. Overall, no differences in disease onset, progression or severity could be detected in mice lacking microglial expression of either one or both of Hdac1 and Hdac2 genes. Similarly, the histopathology showed no differences in lymphocyte or macrophage infiltration or demyelination in either of the analyzed groups. As such, we conclude that unlike in neurodegenerative disease, microglial expression of Hdac1 and Hdac2 does not play a role in EAE.
Highlights
Microglia are the major brain resident type of myeloid cells and play major roles during maturation, homeostasis and various diseases of the central nervous system (CNS) [1,2]
In multiple sclerosis (MS) and animal models of the disease, such as experimental autoimmune encephalomyelitis (EAE), microglia function as part of the immune response
In order to investigate the role of Hdac1 and Hdac2 expression in microglia during neuroinflammatory disease, we the disease courseexpression of experimental autoimmune
Summary
Microglia are the major brain resident type of myeloid cells and play major roles during maturation, homeostasis and various diseases of the central nervous system (CNS) [1,2]. During CNS homeostasis, they continuously survey their surroundings and react to neuronal damage as well as pathogen infiltration. They have been implicated in the regulation of adult neurogenesis as well as synaptic plasticity and myelination [3]. Microglia activation is an essential part of the innate immune response in the otherwise immune-privileged CNS and activated microglia can both serve to remove cellular debris or extracellular protein deposits, such as amyloid plaques, as well as participate in the inflammatory response during CNS disease [2,4]. While activated, ramified microglia can be found predominantly in early active
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
