Frontiers in immunology · 2026
Immunomodulation for stroke-associated pneumonia: a systematic review of mechanistic insight and emerging therapeutic strategies in animal models.
СтатьяСистематический обзорНазвание и аннотация: Перевод в очереди
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Chen Xiangyun, Xu Yihe, Gao Yonghong, Lai Xinxing, Xu Rufan, Zhang Hongrui, Li Na, Liu Zhenhong, Gao Ying
Аннотация
BACKGROUNDS AND AIMS: Stroke-associated pneumonia (SAP) is a major infectious complication that increases mortality after stroke. Stroke-induced immunosuppression has been proposed as a key driver of SAP, supporting the rationale for immunomodulation. This review systematically outlines the immunopathology of SAP and evaluates immune-targeted strategies.
METHODS: Following PRISMA guidelines, we systematically searched PubMed, Scopus, Web of Science, and Embase for studies on the immune mechanisms and immunomodulatory therapies for SAP.
RESULTS: We included 38 studies. Evidence from preclinical models indicates that stroke severity disrupts immune homeostasis, driving SAP through a multi-layered network. Systemic immunosuppression is primarily mediated by sympathetic nervous system (SNS) overactivation, inducing splenic atrophy, lymphocyte apoptosis, and impaired innate immune cells (e.g., iNKT cells), whereas the hypothalamic-pituitary-adrenal (HPA) axis appears to contribute less critically. Furthermore, sustained activation of the cholinergic anti-inflammatory pathway (CAP) may impair pulmonary antimicrobial defense. Active intercellular suppression, as exemplified by monocyte-mediated T cell death, has been identified as a potential mechanism that further compromises immunity. Emerging evidence also implicates disruption of the gut-lung axis (e.g., intestinal barrier dysfunction and microbial dysbiosis), local pulmonary alterations, and dysregulation of key immune molecules (e.g., α-MSH, CD147) as potential contributors to SAP development. Interventions targeting these mechanisms (e.g., iNKT cell activator) have shown promise in preclinical models.
CONCLUSION: This review systematically synthesizes the mechanistic basis of SAP and identifies emerging immunomodulatory interventions. While preclinical evidence is encouraging, most strategies remain experimental, and their clinical translation requires considerable further validation.
METHODS: Following PRISMA guidelines, we systematically searched PubMed, Scopus, Web of Science, and Embase for studies on the immune mechanisms and immunomodulatory therapies for SAP.
RESULTS: We included 38 studies. Evidence from preclinical models indicates that stroke severity disrupts immune homeostasis, driving SAP through a multi-layered network. Systemic immunosuppression is primarily mediated by sympathetic nervous system (SNS) overactivation, inducing splenic atrophy, lymphocyte apoptosis, and impaired innate immune cells (e.g., iNKT cells), whereas the hypothalamic-pituitary-adrenal (HPA) axis appears to contribute less critically. Furthermore, sustained activation of the cholinergic anti-inflammatory pathway (CAP) may impair pulmonary antimicrobial defense. Active intercellular suppression, as exemplified by monocyte-mediated T cell death, has been identified as a potential mechanism that further compromises immunity. Emerging evidence also implicates disruption of the gut-lung axis (e.g., intestinal barrier dysfunction and microbial dysbiosis), local pulmonary alterations, and dysregulation of key immune molecules (e.g., α-MSH, CD147) as potential contributors to SAP development. Interventions targeting these mechanisms (e.g., iNKT cell activator) have shown promise in preclinical models.
CONCLUSION: This review systematically synthesizes the mechanistic basis of SAP and identifies emerging immunomodulatory interventions. While preclinical evidence is encouraging, most strategies remain experimental, and their clinical translation requires considerable further validation.