2016 SOT Tuesday Plenary Session: Mast Cells and Glia: Two Tracks on the Road to Neuroinflammation

Daily Plenary Session: Inflammation and
Neurodegenerative Disease Mast Cells and Glia: Two Tracks on the Road to Neuroinflammation

Lecturer: Stephen Skaper, University of Padua,
Padua, Italy.

One of the more important recent advances
in neuroscience research is the understanding
that there is extensive communication between
the immune system and the central nervous
system (CNS). Proinflammatory cytokines play a key role in this communication. The emerging realization is that glia and microglia, in particular (which are the brain’s resident macrophages), constitute an important source of inflammatory mediators and may have fundamental roles in CNS disorders from neuropathic pain and epilepsy to neurodegenerative diseases. Microglia respond also to proinflammatory signals released from other non-neuronal cells,
principally those of immune origin. Mast cells are of particular relevance in this context. These immune-related cells, while resident in the CNS, are capable of migrating across the blood-spinal cord and blood-brain barriers in situations where the barrier is compromised as a result of CNS pathology. Emerging evidence suggests
the possibility of mast cell-glia communication and opens exciting new perspectives for designing therapies to target neuroinflammation by differentially modulating the activation of non-neuronal cells normally controlling neuronal sensitization, both peripherally and centrally. This presentation will provide an overview of recent
progress relating to the pathobiology of neuroinflammation, the role of microglia, neuroimmune interactions involving mast cells,
in particular, and the possibility that mast cell microglia crosstalk may contribute to the exacerbation of acute symptoms of chronic
neurodegenerative disease and accelerate disease progression, as well as promote pain transmission pathways.