Department of Physiology, Anatomy and Microbiology and Centre for Cardiovascular Biology and Disease Research, School of Life Sciences, La Trobe University, Bundoora, Victoria, Australia.
Department of Physiology, Anatomy and Microbiology and Centre for Cardiovascular Biology and Disease Research, School of Life Sciences, La Trobe University, Bundoora, Victoria, Australia.
Biochem Pharmacol. 2021 Nov;193:114768. doi: 10.1016/j.bcp.2021.114768. Epub 2021 Sep 17.
Ischemic stroke triggers a multifaceted inflammatory response in the brain that contributes to secondary brain injury and infarct expansion. In parallel with brain inflammation, ischemic stroke also leads to post-stroke immunosuppression. Stroke-induced leukopenia then predisposes patients to opportunistic infections potentially leading to pneumonia or unrinary tract infections and a worsened stroke outcome. There is evidence that the hypothalamic-pituitaryadrenal axis plays an important role in the etiology of post-stroke immunosuppression, by which prolonged glucocorticoid signalling leads to changes in immune responses. While opportunistic microbes in hospitals have been thought to be the source of infection, recent studies have reported that gut flora may also be a cause of post-stroke infection as a consequence of compromised integrity of the gut barrier after stroke. While antimicrobial drugs would appear to be a rational form of treatment for bacterial infections in stroke patients, the rise in drug-resistant bacteria and possible adverse effects of disrupting beneficial gut flora represent major challenges with these drugs. Considering the prominent role of gut microbiota in modulating immune responses, protecting and restoring the post-stroke gut bacteriome may provide significant benefit in the context of post-stroke infection. With such broad aspects of post-stroke infection occurring together with an extensive inflammatory response in the brain, a carefully considered administration of therapies for ischemic stroke is warranted.
缺血性脑卒中会在大脑中引发多方面的炎症反应，从而导致继发性脑损伤和梗死扩大。与脑炎症并行的是，缺血性脑卒中还会导致卒中后免疫抑制。卒中引起的白细胞减少症使患者易发生机会性感染，从而导致肺炎或尿路感染，并使卒中预后恶化。有证据表明，下丘脑-垂体-肾上腺轴在卒中后免疫抑制的发病机制中起着重要作用，其中长时间的糖皮质激素信号导致免疫反应的改变。虽然医院中的机会性微生物被认为是感染的来源，但最近的研究报告称，肠道菌群也可能是卒中后感染的原因，因为卒中后肠道屏障的完整性受损。虽然抗菌药物似乎是卒中患者细菌感染的合理治疗形式，但耐药菌的增加以及破坏有益肠道菌群的可能不良反应，是这些药物面临的主要挑战。考虑到肠道微生物群在调节免疫反应方面的重要作用，保护和恢复卒中后的肠道细菌组可能会为卒中后感染提供显著的益处。由于卒中后感染涉及到如此广泛的方面，以及大脑中广泛的炎症反应，因此有必要对缺血性脑卒中的治疗进行仔细考虑。
