Identification of the endogenous signals initiating inflammation and tissue damage in the injured spinal cord
Funded in: 2011, 2012, 2013
Back to overview
Although necrosis is the principal mechanism of cell death at sites of SCI, studies have demonstrated the existence of delayed apoptotic cell loss in a process now referred to as secondary degeneration. While preventing much of the rapid death of neural cells undergoing necrosis is unrealistic, strategies aimed at preventing secondary degeneration clearly represent a potentially effective therapeutic means for SCI victims. Evidence that has accumulated over the years suggests that blood-derived immune cells that are attracted at sites of SCI may act as mediators of secondary degeneration.
Interleucines (IL) modulate the synthesis and release of chemokines that trigger the recruitment of aggressive immune cells, at sites of injury, thereby contributing to secondary damage.
Previous data show that chemokine expression and the infiltration of these aggressive immune cells at sites of SCI are severely impaired in mice deficient for IL receptors, resulting in a better functional recovery after SCI.
Aims of the project are:
- to further define the endogenous signals involved in the initiation of inflammation after SCI
- to put in place imaging protocols that will allow to study, in real time in vivo, the contribution of blood-derived immune cells to neuronal and myelin damage and test the efficacy of anti-IL-1 therapies longitudinally