Stroke-Associated Pneumonia and the Brain-Gut-Lung Axis

BACKGROUND: Stroke-associated pneumonia (SAP), a highly lethal complication following stroke, is closely linked to dysregulation of the "brain-gut-lung axis." Accumulating evidence indicates that stroke triggers intestinal alterations through the brain-gut axis, while multiple studies confirm that gut-derived changes can mediate pneumonia through the gut-lung axis. However, the mechanisms connecting stroke-induced intestinal dyshomeostasis to SAP remain incompletely elucidated, and the multiorgan interaction mechanisms of the "brain-gut-lung axis" in SAP pathogenesis require further exploration. REVIEW SUMMARY: This systematic literature review systematically searched databases, including PubMed, using the keywords "stroke," "gastrointestinal microbiome," and "bacterial pneumonia," incorporating 80 mechanistic studies. Key findings reveal that stroke initiates a cascade of "neuro-microbial-immune" pathway interactions along the brain-gut-lung axis, leading to intestinal dyshomeostasis characterized by microbiota and metabolite alterations, barrier disruption, immune dysregulation, inflammatory responses, and impaired gut motility. These intestinal perturbations ultimately disrupt pulmonary immune homeostasis, promoting SAP development. In addition, stroke directly induces vagus nerve injury through the brain-gut axis, resulting in impaired swallowing and cough reflexes that exacerbate aspiration-related pulmonary infection risks. CONCLUSIONS: Elucidating the role of the brain-gut-lung axis in SAP pathogenesis provides critical insights into its underlying mechanisms. This paradigm highlights intestinal homeostasis modulation and vagus nerve stimulation as promising therapeutic strategies for SAP prevention and management, advancing a multitargeted approach to mitigate poststroke complications.