We utilize a model of neuroinflammation induced by exposure to repetitive episodes of hypoxia (intermittent hypoxia). We flow gases through the housing cages using a custom-designed, computer controlled system.

To investigate mechanisms of microglial plasticity, we employ a multi-disciplinary approach including in vivo and in vitro assays. We use quantitative RT-PCR, immunoblot, ELISA, chromatin immunoprecipitation (ChIP), immunohistochemistry (left), flow cytometry (right) and tissue culture to assess microglial signaling, cytokine and growth factor production, and gene expression.

Current studies utilize RNASeq and whole genome ChIPSeq to determine how the microglial transcriptome is influenced by intermittent hypoxia, and how exposure to this chronic neuroinflammatory stimulus alters post-translational modifications of histones, respectively.

Microglia comprise 5-10% of all CNS cells. Thus, to study their activities in vivo, we must distinguish them from the other more abundant CNS cell types (i.e. neurons and astrocytes). We do this by positively selecting for microglia using immunomagnetic cell sorting (left) or flow cytometry (middle). From these sorted cell populations we can then analyze nucleic acids (mRNA, miRNA and DNA; right) and histone modifications to determine how microglial responses are altered during neuroinflammation.