Shows that gut dysbiosis worsens stroke severity, suggesting microbiota-targeted interventions may help.
Gut microbiota has emerged as a key regulator of immune, metabolic, and neuroinflammatory processes, exerting significant influence on central nervous system (CNS) function via the gut-brain axis. Growing evidence suggests that gut dysbiosis not only precedes and worsens stroke severity but is also induced by stroke itself, establishing a bidirectional and self-reinforcing pathological loop. Microbiota-derived metabolites, including short-chain fatty acids and tryptophan derivatives, modulate the activation states of microglial and border-associated macrophage (BAMs), thereby shaping neuroinflammatory responses and tissue repair mechanisms. Although microglia have been extensively studied in this context, the role of BAMs-particularly perivascular-macrophages remains comparatively underexplored, despite their critical involvement in maintaining blood-brain barrier (BBB) integrity and immune surveillance. In addition, dietary patterns strongly influence microbiota composition and, consequently, immune responses within the CNS. Collectively, these findings position gut microbiota as a dynamic regulator of brain-resident immune cells in stroke and highlight diet- and microbiota-targeted interventions as promising therapeutic strategies.
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Santos et al. (2026) studied this question.
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