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<p>In human, decompressive craniectomy (DC) reduces morbi-mortality of malignant stroke. Because the cranial vault carries hematopoietic niches hosting inflammatory cells, we used here a preclinical model of stroke and DC in mice to evaluate whether the removal of the cranial vault may influence neuroinflammation after malignant stroke. 99 C57/BL6 mice were used, and stroke was induced using a filament model. Mice were randomized in 4 groups: Sham (<i>n</i> = 15), Stroke (<i>n</i> = 40), DC (<i>n</i> = 18) and Stroke + DC (<i>n</i> = 26). The inflammatory response was evaluated at D1 and D5 by using both non-invasive molecular MRI of VCAM-1 signal void and flow cytometry analyses of a large set of immune cells. Molecular MRI of VCAM-1 revealed a massive endothelial inflammatory status after stroke, a process reduced by DC at day 1 and day 5. We also revealed that DC reduced levels of border-associated macrophages (BAMs) induced by stroke in the ipsilateral hemisphere, which was associated with an increase of BAMs in the contralateral hemisphere. Effect on inflammatory processes in the contralateral hemisphere was also confirmed by a decrease of parenchymal T-cells (CD3<sup>+</sup>) in the DC group as compared to the Stroke group. DC reduces post-stroke cerebral inflammation, as shown by molecular MRI, and may modulate BAM and parenchymal T-cell distribution.</p>

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Decompressive Craniectomy Decreases Neuroinflammation after Ischemic Stroke in Mice

  • 期刊论文

  • 发表日期：

    2026年3月16日

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  • Josephine Malczuk,
  • Jonathane Furon,
  • Emmie Coué,
  • Maxime Gauberti,
  • Lucile Sandberg,
  • Anthony Levilly,
  • Alin Borha,
  • Evelyne Emery,
  • Denis Vivien,
  • Thomas Gaberel

摘要

In human, decompressive craniectomy (DC) reduces morbi-mortality of malignant stroke. Because the cranial vault carries hematopoietic niches hosting inflammatory cells, we used here a preclinical model of stroke and DC in mice to evaluate whether the removal of the cranial vault may influence neuroinflammation after malignant stroke. 99 C57/BL6 mice were used, and stroke was induced using a filament model. Mice were randomized in 4 groups: Sham (n = 15), Stroke (n = 40), DC (n = 18) and Stroke + DC (n = 26). The inflammatory response was evaluated at D1 and D5 by using both non-invasive molecular MRI of VCAM-1 signal void and flow cytometry analyses of a large set of immune cells. Molecular MRI of VCAM-1 revealed a massive endothelial inflammatory status after stroke, a process reduced by DC at day 1 and day 5. We also revealed that DC reduced levels of border-associated macrophages (BAMs) induced by stroke in the ipsilateral hemisphere, which was associated with an increase of BAMs in the contralateral hemisphere. Effect on inflammatory processes in the contralateral hemisphere was also confirmed by a decrease of parenchymal T-cells (CD3+) in the DC group as compared to the Stroke group. DC reduces post-stroke cerebral inflammation, as shown by molecular MRI, and may modulate BAM and parenchymal T-cell distribution.