Bai Jing, Zhao Yusheng, Wang Zihe, Qin Peng, Huang Jingjie, Cheng Yupei, Wang Chaoran, Chen Yuyan, Liu Longxiao, Zhang Yuxing, Wu Bangqi
Tianjin University of Traditional Chinese Medicine.
National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion, First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Neurologist. 2025 May 7. doi: 10.1097/NRL.0000000000000626.
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.
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.
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.
卒中相关性肺炎（SAP）是卒中后一种具有高度致死性的并发症，与“脑-肠-肺轴”的失调密切相关。越来越多的证据表明，卒中通过脑-肠轴引发肠道改变，而多项研究证实，源自肠道的变化可通过肠-肺轴介导肺炎。然而，将卒中诱导的肠道内环境稳态失衡与SAP联系起来的机制仍未完全阐明，“脑-肠-肺轴”在SAP发病机制中的多器官相互作用机制需要进一步探索。
本系统文献综述使用关键词“卒中”“胃肠道微生物组”和“细菌性肺炎”，系统检索了包括PubMed在内的数据库，纳入了80项机制研究。主要发现表明，卒中沿脑-肠-肺轴引发一系列“神经-微生物-免疫”途径相互作用，导致以微生物群和代谢物改变、屏障破坏、免疫失调、炎症反应和肠道蠕动受损为特征的肠道内环境稳态失衡。这些肠道紊乱最终破坏肺部免疫稳态，促进SAP的发展。此外，卒中通过脑-肠轴直接诱导迷走神经损伤，导致吞咽和咳嗽反射受损，加剧与误吸相关的肺部感染风险。
阐明脑-肠-肺轴在SAP发病机制中的作用，为其潜在机制提供了关键见解。这一范式强调肠道内环境稳态调节和迷走神经刺激是预防和管理SAP的有前景的治疗策略，推动了一种多靶点方法来减轻卒中后并发症。
