engleski

Lateral fluid percussion injury in the rat instigates early T-cell infiltration in the ipsilateral parietal cortex

Introduction: Traumatic brain injury (TBI) represents a burden to healthcare due to limited management options and long-term consequences. The latter are underrepresented and contribute to naming TBI a “silent epidemic“. Neuroinflammation appears to have a significant role in the development of secondary brain injury, involving processes affecting both resolution and persistence of inflammation. The purpose of this study was to illustrate the early activation of the cell-mediated response in experimental model of TBI. Methods: Lateral fluid percussion injury (LFPI), a TBI model causing both focal cortical lesion and diffuse damage in the ipsilateral hemisphere, was induced in adult male Wistar rats. Sham-operated rats were used as a control group. Animals were sacrificed 1, 3, or 7 days following the procedure. Markers of the cellular arm of adaptive immunity, CD+ cells, were evaluated by quantitative and qualitative immunohistochemical and immunofluorescent analyses of the brain tissue. Results: The results of this study demonstrate the invasion of CD3+, CD4+, and CD8+ cells in the ipsilateral cortices of the brain-injured animals. The number of CD3+ cells significantly increased 1 day after the trauma and has decreased towards the 8th day. Furthermore, CD4+ cells were most abundantly present in the cortex 3 days after the injury. Invasion of CD8+ cells was also noted not only in the cortex but also in the ipsilateral subpial space. Conclusion: Reported results show that LFPI elicits cellular immune response in the first days following TBI, which could modulate secondary events following the trauma and determining recovery outcome. This work was fully supported by project uniri- biomed-18-204 to Prof Gordana Župan.

adaptive immunity ; immunity, cellular ; neuroinflammation ; rats ; traumatic brain injury

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