Ischemic stroke is a highly complex systemic disease characterized by intricate interactions between the brain and gastrointestinal tract. While our current understanding of these interactions primarily stems from experimental models, their relevance to human stroke outcomes is of considerable interest. After stroke, bidirectional communication between the brain and gastrointestinal tract initiates changes in the gastrointestinal microenvironment. These changes involve the activation of gastrointestinal immunity, disruption of the gastrointestinal barrier, and alterations in gastrointestinal microbiota. Importantly, experimental evidence suggests that these alterations facilitate the migration of gastrointestinal immune cells and cytokines across the damaged blood-brain barrier, ultimately infiltrating the ischemic brain. Although the characterization of these phenomena in humans is still limited, recognizing the significance of the brain-gastrointestinal crosstalk after stroke offers potential avenues for therapeutic intervention. By targeting the mutually reinforcing processes between the brain and gastrointestinal tract, it may be possible to improve the prognosis of ischemic stroke. Further investigation is warranted to elucidate the clinical relevance and translational potential of these findings.