Westendorp Willeke F, Dames Claudia, Nederkoorn Paul J, Meisel Andreas
Department of Neurology, Amsterdam Neuroscience, University of Amsterdam, the Netherlands (W.F.W., P.J.N.).
Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Klinik für Neurologie mit Experimenteller Neurologie, Center for Stroke Research Berlin, NeuroCure Clinical Research Center, Germany (C.D., A.M.).
Stroke. 2022 May;53(5):1438-1448. doi: 10.1161/STROKEAHA.122.038867. Epub 2022 Mar 28.
Stroke remains one of the main causes of mortality and morbidity worldwide. Immediately after stroke, a neuroinflammatory process starts in the brain, triggering a systemic immunodepression mainly through excessive activation of the autonomous nervous system. Manifestations of immunodepression include lymphopenia but also dysfunctional innate and adaptive immune cells. The resulting impaired antibacterial defenses render patients with stroke susceptible to infections. In addition, other risk factors like stroke severity, dysphagia, impaired consciousness, mechanical ventilation, catheterization, and older age predispose stroke patients for infections. Most common infections are pneumonia and urinary tract infection, both occur in ≈10% of the patients. Especially pneumonia increases unfavorable outcome and mortality in patients with stroke; systemic effects like hypotension, fever, delay in rehabilitation are thought to play a crucial role. Experimental and clinical data suggest that systemic infections enhance autoreactive immune responses against brain antigens and thus negatively affect outcome but convincing evidence is lacking. Prevention of poststroke infections by preventive antibiotic therapy did not improve functional outcome after stroke. Immunomodulatory approaches counteracting immunodepression to prevent stroke-associated pneumonia need to account for neuroinflammation in the ischemic brain and avoid further tissue damage. Experimental studies discovered interesting targets, but these have not yet been investigated in patients with stroke. A better understanding of the pathobiology may help to develop optimized approaches of preventive antibiotic therapy or immunomodulation to effectively prevent stroke-associated pneumonia while improving long-term outcome after stroke. In this review, we aim to characterize epidemiology, risk factors, cause, diagnosis, clinical presentation, and potential treatment of poststroke immunosuppression and associated infections.
中风仍然是全球范围内主要的死亡和发病原因之一。中风后，大脑立即启动神经炎症过程，主要通过自主神经系统的过度激活引发全身免疫抑制。免疫抑制的表现包括淋巴细胞减少，以及先天性和适应性免疫细胞功能失调。由此导致的抗菌防御受损使中风患者易受感染。此外，中风严重程度、吞咽困难、意识障碍、机械通气、插管和高龄等其他风险因素也使中风患者易发生感染。最常见的感染是肺炎和尿路感染，两者在约10%的患者中发生。尤其是肺炎会增加中风患者的不良结局和死亡率；低血压、发热、康复延迟等全身影响被认为起着关键作用。实验和临床数据表明，全身感染会增强针对脑抗原的自身反应性免疫反应，从而对结局产生负面影响，但缺乏确凿证据。预防性抗生素治疗预防中风后感染并未改善中风后的功能结局。对抗免疫抑制以预防中风相关性肺炎的免疫调节方法需要考虑缺血性脑中的神经炎症，并避免进一步的组织损伤。实验研究发现了有趣的靶点，但尚未在中风患者中进行研究。更好地理解病理生物学可能有助于开发优化的预防性抗生素治疗或免疫调节方法，以有效预防中风相关性肺炎，同时改善中风后的长期结局。在本综述中，我们旨在描述中风后免疫抑制及相关感染的流行病学、风险因素、病因、诊断、临床表现和潜在治疗方法。
