4.2. Inflammatory reaction

During an early phase after SCI, interleukins (IL-6, IL-1β), cyclooxygenase (COX)-2 and TNF-α are activated, which get to normal stage again after 2 weeks. Integrins, vascular and intercellular CAMs, selectins and cadherins are upregulated in early phase of SCI [25]. Inflammatory genes are expressed in several spinal cord cells, which are predominantly studied in microglia. The interleukins IL-6, IL-1β and chemokine ligands, such as 2/M1P2α and 2/MCP-1, help in bringing different immune cells to the injured area [14]. After 3–7 days, microglial gene expression that includes genes, such as MRF-1 (microglial response factor-1), cathepsin, galectin-3, CYBA (cytochrome b-245, alpha polypeptide), CASP1 (caspase 1), MAPK14 (mitogenactivated protein kinase 14), CCND1 (cyclin D1) and leukocyte surface antigen CD53/OX44, contributes in immune response, phagocytosis and cell death. Furthermore, other genes such as the classical complement pathway, which related to phagocytosis, showed an insistent upregulation after SCI [25].
