Department of Neurology, Rigshospitalet, Glostrup, Denmark.
Biotech Research and Innovation Center, University of Copenhagen, Copenhagen, Denmark.
Int J Neurosci. 2024 Jun;134(2):197-205. doi: 10.1080/00207454.2022.2098733. Epub 2022 Jul 15.
Infections are frequent complications in acute ischemic stroke and may be caused by an altered immune response influencing brain damage. We compared long-term immune responses in stroke patients with or without infections during the recovery period by performing a long-term profiling of clinically relevant inflammatory parameters from stroke onset until day 49.
Thirty-four stroke patients were retrospectively included and divided into two groups depending on infection status. Group 1 had no infections ( = 17) and group 2 had post-admission infection ( = 17). The patients were evaluated carefully for infections and evolution of the peripheral inflammatory response. Neutrophils, monocytes, lymphocytes, total leukocytes and C-reactive protein were evaluated in relation to the occurrence and development of infections. In both patient groups, an acute boost in neutrophils and monocytes were observed whereas the opposite was true for lymphocytes.
In Group 1, neutrophils and monocytes approached normal levels after 20-30 days, but remained elevated in Group 2. We found an increase in neutrophils ( = 0.01) and leukocytes ( < 0.01) as well as C-reactive protein ( < 0.01) among infected patients. Lymphocytes remained depressed in Group 2, while Group 1 slowly approached baseline levels. In both groups, CRP levels initially increased with a slow return to baseline levels. From day 0 to 49 after stroke, uninfected patients generally experienced a decline in leukocytes, neutrophils and monocytes (all < 0.05), while no similar changes happened among infected patients.
Our study provides an overview of general immune cell kinetics after stroke related to infection status. Immune cell numbers were severely disturbed for weeks after the insult, independent of infection status, although infected patients achieved the highest cell counts of neutrophils, leukocytes and for C-reactive protein. The sustained depression of lymphocytes, especially and paradoxically among infected patients, warrants future studies into the mechanisms behind this, with potential for future therapies aimed at restoring normal immunity and thereby improving patient outcome.
感染是急性缺血性脑卒中的常见并发症，可能是由于改变的免疫反应影响脑损伤所致。我们通过对脑卒中发病至第 49 天的临床相关炎症参数进行长期分析，比较了恢复期有无感染的脑卒中患者的长期免疫反应。
回顾性纳入 34 例脑卒中患者，根据感染情况分为两组。第 1 组无感染（n=17），第 2 组发生入院后感染（n=17）。仔细评估患者感染情况和外周炎症反应的演变。评估中性粒细胞、单核细胞、淋巴细胞、白细胞总数和 C 反应蛋白与感染发生和发展的关系。在两组患者中，均观察到中性粒细胞和单核细胞的急性增加，而淋巴细胞则相反。
第 1 组中，中性粒细胞和单核细胞在 20-30 天后接近正常水平，但第 2 组仍升高。我们发现感染患者的中性粒细胞（=0.01）和白细胞（<0.01）以及 C 反应蛋白（<0.01）增加。第 2 组的淋巴细胞仍然减少，而第 1 组则缓慢接近基线水平。在两组中，CRP 水平最初升高，然后缓慢恢复到基线水平。从脑卒中后第 0 天到第 49 天，未感染患者的白细胞、中性粒细胞和单核细胞普遍下降（均<0.05），而感染患者则无类似变化。
本研究提供了感染状态相关的脑卒中后一般免疫细胞动力学的概述。免疫细胞数量在损伤后数周内受到严重干扰，与感染状态无关，尽管感染患者的中性粒细胞、白细胞和 C 反应蛋白计数最高。特别是感染患者的淋巴细胞持续减少，这令人深思，值得进一步研究潜在的机制，以期未来开发针对恢复正常免疫的治疗方法，从而改善患者预后。
