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Background <p>Traumatic brain injury (TBI) triggers neuroinflammation both acutely and chronically, the latter which might be involved in neurodegenerative disorders. Resolvins are neuroinflammatory modulators, hypothesized to improve resolution of inflammation. This study sought to explore sustained immunological responses after delayed treatment with resolvins utilizing novel tools for automated cellular assessments.</p> Materials and methods <p>Twenty-five rodents (Sprague-Dawley rats) were exposed to a penetrating TBI, following which delayed treatment with resolvin was initiated. Assessments of tissue loss, and persistent neuroinflammatory activation, was assessed at 6 weeks post-injury utilizing histological and immunohistochemical methods. We also developed a novel computational tool to count and automatically assess cell counts across treatment groups.</p> Results <p>The TBI model elicited a substantial brain injury, as expected. The lesion cavity volume was not affected by resolvin or vehicle treatment. Notably, both microglial and macrophage responses were also similar between treatment groups, as deemed by state-of-the-art computational models.</p> Conclusion <p>Resolvins administered in a delayed fashion following severe TBI did not affect the extent of chronic microglial or macrophage responses, but warrants future corroboration. Dosing and timing of resolvin treatment warrants further study.</p>

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Immunological response and tissue loss in a rodent model of chronic traumatic brain injury treated with resolvin

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年10月2日

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  • Olivia Kiwanuka,
  • Julie Cheung,
  • Anders Hånell,
  • Caroline Lindblad

摘要

Background

Traumatic brain injury (TBI) triggers neuroinflammation both acutely and chronically, the latter which might be involved in neurodegenerative disorders. Resolvins are neuroinflammatory modulators, hypothesized to improve resolution of inflammation. This study sought to explore sustained immunological responses after delayed treatment with resolvins utilizing novel tools for automated cellular assessments.

Materials and methods

Twenty-five rodents (Sprague-Dawley rats) were exposed to a penetrating TBI, following which delayed treatment with resolvin was initiated. Assessments of tissue loss, and persistent neuroinflammatory activation, was assessed at 6 weeks post-injury utilizing histological and immunohistochemical methods. We also developed a novel computational tool to count and automatically assess cell counts across treatment groups.

Results

The TBI model elicited a substantial brain injury, as expected. The lesion cavity volume was not affected by resolvin or vehicle treatment. Notably, both microglial and macrophage responses were also similar between treatment groups, as deemed by state-of-the-art computational models.

Conclusion

Resolvins administered in a delayed fashion following severe TBI did not affect the extent of chronic microglial or macrophage responses, but warrants future corroboration. Dosing and timing of resolvin treatment warrants further study.