Varvel lab · Pharmacology and Chemical Biology, Emory University School of Medicine
Peripheral myeloid EP2 activation after status epilepticus
Status epilepticus is followed by inflammation that does not simply accompany the injury but contributes to it. The question this line of work asks is which cells are responsible — brain-resident microglia, or myeloid cells recruited from the periphery — because only one of those is reachable by a drug that does not cross into the brain.
Status. Work in Dr. Nicholas Varvel's laboratory at Emory. Published as Varvel NH, Espinosa-Garcia C, Hunter-Chang S, et al., Journal of Neuroscience 2021;41(5):1105–1117.
This hub is still being built. The analysis is underway; the derivation, tables and figures will be posted here as they are finished, the way the completed projects on this site are. What is below is the design and the current state, written up as it stands.
The question
How much of the damaging inflammatory response after status epilepticus is driven by EP2 activation on peripheral myeloid cells rather than on brain-resident cells?
How it is being done
- Mouse models of status epilepticus with genetic and pharmacologic manipulation of EP2 signalling.
- Gene expression and PCR-based readouts of the inflammatory response.
- Separation of peripheral myeloid contribution from brain-resident microglial contribution.
Materials
About & provenance
I am not an author on the published paper; this page describes the laboratory project I worked on, with the publication cited as its outcome.
This page grows as the work does.