Role of MIP-1alpha (CCL3) and its receptors after spinal cord injury and its influence on secondary damage
Funded in: 2016, 2017, 2018
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Problem: After spinal cord injury (SCI), secondary processes like inflammation and bleeding cause additional tissue loss
Target: Evaluation of the chemokine CCL3 after SCI
Goal: This could lead to a new therapeutic approach to reduce secondary damage
Tissue damage after spinal cord injury (SCI) occurs as primary damage, which is caused by the mechanical trauma, and is followed by secondary damage, which is a process mediated by factors including inflammation and bleeding. Reduction of this secondary damage would directly affect the size of the tissue damage and thereby the extent of the functional deficit.
Red blood cells are present in the injured spinal cord tissue due to bleeding. When immune cells take them up, these cells can produce messenger factors (cytokines and chemokines) that influence other cells to maintain inflammation and destruct more tissue. One of these factors is CCL3.
The focus of this project is to investigate the role of CCL3 in a mouse model of contusional SCI, to determine when and where it is present, how its presence influences the inflammatory process and if modulation can reduce tissue damage.
If successful, this work will lead to a better understanding of secondary tissue damage and immune cell activation after SCI and could potentially be a target for a therapeutic approach.