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Background <p>Stroke is a complex and highly heterogeneous acute cerebrovascular disease characterized by high incidence, disability rates, and mortality. The occurrence of a stroke is the result of a series of chain reactions. Neuroinflammation, as a core component of the pathological process of stroke, serves as the dynamic hub of this chain of reactions. It acts both as a driving force in disease progression and a key regulator of functional recovery. Increasing evidence indicates that the gut microbiota has a dynamic coupling relationship with the neuroinflammatory pathological processes involved in stroke. This review aimed to explore the mechanisms by which the gut microbiota influences neuroinflammation following stroke and to evaluate its therapeutic potential in stroke.</p> Main body <p>Following a stroke, up to 50% of patients have pathophysiological changes in the gastrointestinal tract, which are closely associated with delayed recovery, increased mortality, and worsened neurological outcomes. The gut microbiota can modulate post-stroke neuroinflammation through multiple pathways, including immune regulation (innate and adaptive immunity), neural signal transmission (vagus nerve and enteric nervous system), neuroendocrine transmission (hypothalamus-pituitary-adrenal axis), and gut microbiota metabolite pathways. This “central-peripheral-central” feedback loop is considered a potential intervention target. In this review, we summarized the characteristics of gut microbiota alterations following stroke, elucidated its mechanisms of action in neuroinflammation, and explored gut microbiota-based intervention strategies and their limitations. Finally, we proposed directions to provide new insights and references for clinical translation for the prevention and treatment of stroke.</p> Conclusions <p>The gut microbiota plays a key role in post-stroke pathology. The gut microbiota modulates the onset and progression of post-stroke neuroinflammation through multidimensional mechanisms via the “immune-neuro-endocrine” feedback pathway at multiple levels. Interventions targeting the gut microbiota can not only suppress excessive inflammation but also repair neural networks, ultimately improving functional outcomes after stroke.</p> Graphical Abstract <p></p>

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Gut microbiota-mediated neuroinflammation following stroke: mechanisms and intervention strategies

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月30日

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  • Lili Teng,
  • Minmin Wu,
  • Wenjing Song,
  • Qingmei Wang,
  • Xun Luo,
  • Luwen Zhu

摘要

Background

Stroke is a complex and highly heterogeneous acute cerebrovascular disease characterized by high incidence, disability rates, and mortality. The occurrence of a stroke is the result of a series of chain reactions. Neuroinflammation, as a core component of the pathological process of stroke, serves as the dynamic hub of this chain of reactions. It acts both as a driving force in disease progression and a key regulator of functional recovery. Increasing evidence indicates that the gut microbiota has a dynamic coupling relationship with the neuroinflammatory pathological processes involved in stroke. This review aimed to explore the mechanisms by which the gut microbiota influences neuroinflammation following stroke and to evaluate its therapeutic potential in stroke.

Main body

Following a stroke, up to 50% of patients have pathophysiological changes in the gastrointestinal tract, which are closely associated with delayed recovery, increased mortality, and worsened neurological outcomes. The gut microbiota can modulate post-stroke neuroinflammation through multiple pathways, including immune regulation (innate and adaptive immunity), neural signal transmission (vagus nerve and enteric nervous system), neuroendocrine transmission (hypothalamus-pituitary-adrenal axis), and gut microbiota metabolite pathways. This “central-peripheral-central” feedback loop is considered a potential intervention target. In this review, we summarized the characteristics of gut microbiota alterations following stroke, elucidated its mechanisms of action in neuroinflammation, and explored gut microbiota-based intervention strategies and their limitations. Finally, we proposed directions to provide new insights and references for clinical translation for the prevention and treatment of stroke.

Conclusions

The gut microbiota plays a key role in post-stroke pathology. The gut microbiota modulates the onset and progression of post-stroke neuroinflammation through multidimensional mechanisms via the “immune-neuro-endocrine” feedback pathway at multiple levels. Interventions targeting the gut microbiota can not only suppress excessive inflammation but also repair neural networks, ultimately improving functional outcomes after stroke.

Graphical Abstract