Neuroinflammatory Trafficking During Acute Viral Infection of the Brain

The lab's research into neuroinflammatory trafficking during acute viral infection of the brain addresses fundamental issues in host response to acute viral infection. The research goal is to drive novel therapeutic strategies for protecting the brain and modulating the immune response in autoimmune and neuroinflammatory diseases.

Acute viral infection of the central nervous system is a significant cause of morbidity and mortality, especially in children and older adults. The mechanisms of neural injury during such infection are unclear, preventing the development of neuroprotective strategies that will preserve cognitive function.

To discover the mechanisms of neural injury mediated by the inflammatory response to acute infection, the lab uses an animal model of picornavirus infection that has revealed a key role for innate effector cells. Critically, this model also provides insight into the basic mechanisms of antigen trafficking from the brain to the peripheral adaptive immune system.

Focus areas include:

  • Using novel reporter mice to discover the chemotactic factors required for recruitment of inflammatory monocytes into the acutely infected brain
  • Characterizing the mechanisms of neuronal injury induced by infiltrating inflammatory monocytes
  • Using live animal multiphoton imaging to discover the factors that control inflammatory monocyte egress from the brain and subsequent trafficking to the peripheral lymph nodes
  • Identifying the role of inflammatory monocytes in antigen presentation and shaping of the adaptive antiviral immune response
  • Using high-parameter flow cytometry to characterize the phenotypic changes that occur in infiltrating inflammatory monocytes during migration through the brain
  • Development of more-sophisticated live animal 4-D imaging tools for the analysis of cellular trafficking in the brain and cervical lymph nodes