Abstract

Our study of the changes in cytokine profile in blood serum and in the spinal cord after traumatic spinal cord injury (SCI) has shown that an inflammatory reaction and immunological response are not limited to the CNS, but widespread. This fact was confirmed by changes detected in a cytokine profile in blood serum samples [MIP-1α, interleukin 1 (IL-1) α, IL-2, IL-5, IL-1β, MCP-1, RANTES]. There were also changes in the levels of MIP-1α, IL-1α, IL-2, IL-5, IL-18, GM-colony-stimulating factor, IL-17α, IFN-γ, IL-10, IL-13, MCP-1, and GRO KC CINC-1 in samples of the rat injured spinal cord. The results underscore the complex cytokine network imbalance exhibited after SCI and show significant changes in the concentrations of 14 cytokines/chemokines with different inflammatory and immunological activities.

Highlights

  • The treatment results of patients with traumatic spinal cord injury (SCI) are extremely poor

  • The assessment of the cytokine profile in the site of SCI at different periods after contusion injury showed a significant change in concentrations of cytokines/chemokines such as MIP-1α, interleukin 1 (IL-1) α, IL-2, IL-5, IL-18, GM-colony-stimulating factor (CSF), IL-17α, IFN-γ, IL-10, IL-13, MCP-1, and GRO KC CINC-1 (Table 2; Figure 1)

  • On 7 and 14 dpi, there was a decrease in MIP-1α concentrations compared with the values on day 3; the values still exceeded those in the intact controls by 4.42 and 5.6 times, respectively (P < 0.05)

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Summary

Introduction

The treatment results of patients with traumatic spinal cord injury (SCI) are extremely poor. This field requires the development and implementation of new therapeutic protocols. Inflammation and tissue infiltration by various immune cells, which can penetrate into the spinal cord tissue through damage to the blood–brain barrier, play a significant role in the pathogenesis of secondary damage. At the site of inflammation there is an immunological dysfunction, of which the cause is still unclear. Inflammatory processes lead to a systemic reaction and trigger an immune response that can potentially cause an autoimmune reaction similar to that of multiple sclerosis and central nervous system lesions in systemic lupus erythematosus. The question whether immune processes have a more positive or negative impact on regeneration is still a matter of discussion [1]

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