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<p>Ischemic brain injury triggers complex immune-inflammatory responses that significantly influence disease progression and patient outcomes. This study investigates the role of heat shock protein A8 (<i>Hspa8</i>) in modulating immune cell dynamics following ischemic brain injury. Using single-cell RNA sequencing, bulk RNA sequencing, flow cytometry, and immunofluorescence, we identified significant alterations in T cells, neutrophils, and monocytes within both peripheral blood and brain tissues. Our findings reveal that <i>Hspa8</i> plays a pivotal role in regulating neutrophil infiltration and reactive oxygen species (ROS) production. Gene silencing of <i>Hspa8</i> effectively reduced neutrophil accumulation, decreased ROS levels, and mitigated neurological deficits in both in vitro and in vivo ischemic models. Protein-protein interaction (PPI) network analysis further established <i>Hspa8</i> as a key regulator in immune cell interactions, highlighting its potential as a therapeutic target. These results provide new insights into the immune mechanisms underlying ischemic brain injury and suggest that targeting <i>Hspa8</i> may offer a promising strategy for reducing inflammation, improving neurological recovery, and enhancing clinical outcomes in affected patients.</p><p></p>

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Hspa8 modulation of immune responses mitigates ischemic brain injury

  • 期刊论文

  • 发表日期：

    2025年11月1日

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  • Xiaokun Wu,
  • Zongkai Wu,
  • Han Yan,
  • Zhe Zu,
  • Hebo Wang

摘要

Ischemic brain injury triggers complex immune-inflammatory responses that significantly influence disease progression and patient outcomes. This study investigates the role of heat shock protein A8 (Hspa8) in modulating immune cell dynamics following ischemic brain injury. Using single-cell RNA sequencing, bulk RNA sequencing, flow cytometry, and immunofluorescence, we identified significant alterations in T cells, neutrophils, and monocytes within both peripheral blood and brain tissues. Our findings reveal that Hspa8 plays a pivotal role in regulating neutrophil infiltration and reactive oxygen species (ROS) production. Gene silencing of Hspa8 effectively reduced neutrophil accumulation, decreased ROS levels, and mitigated neurological deficits in both in vitro and in vivo ischemic models. Protein-protein interaction (PPI) network analysis further established Hspa8 as a key regulator in immune cell interactions, highlighting its potential as a therapeutic target. These results provide new insights into the immune mechanisms underlying ischemic brain injury and suggest that targeting Hspa8 may offer a promising strategy for reducing inflammation, improving neurological recovery, and enhancing clinical outcomes in affected patients.