Faculty of Biology, University of Warsaw, Miecznikowa 1, 02-096 Warszawa, Poland.
Faculty of Chemistry, Nicolaus Copernicus in Toruń, Gagarina 7, 87-100 Toruń, Poland.
Int J Mol Sci. 2023 Sep 12;24(18):13994. doi: 10.3390/ijms241813994.
Parasitic helminths induce a transient, short-term inflammation at the beginning of infection, but in persistent infection may suppress the systemic immune response by enhancing the activity of regulatory M2 macrophages. The aim of the study was to determine how nematode infection affects age-related neuroinflammation, especially macrophages in the nervous tissue. Here, intraperitoneal LPS-induced systemic inflammation resulting in brain neurodegeneration was enhanced by prolonged infection in C57BL/6 mice. The changes in the brain coincided with the increase in M1 macrophages, reduced survivin level, enhanced APP and GFAP expression, chitin-like chains deposition in the brain and deterioration behaviour manifestations. These changes were also observed in transgenic C57BL/6 mice predisposed to develop neurodegeneration typical for Alzheimer's disease in response to pathogenic stimuli. Interestingly, in mice infected with the nematode only, the greater M2 macrophage population resulted in better results in the forced swim test. Given the growing burden of neurodegenerative diseases, understanding such interactive associations can have significant implications for ageing health strategies and disease monitoring.
寄生虫性蠕虫在感染初期会引发短暂的短期炎症，但在持续性感染中，可能通过增强调节性 M2 巨噬细胞的活性来抑制全身免疫反应。本研究旨在确定线虫感染如何影响与年龄相关的神经炎症，特别是神经组织中的巨噬细胞。在这里，通过延长 C57BL/6 小鼠的感染，腹腔内 LPS 诱导的全身性炎症导致大脑神经退行性变加剧。大脑的变化与 M1 巨噬细胞的增加、生存素水平降低、APP 和 GFAP 表达增强、大脑中几丁质样链沉积以及行为表现恶化相一致。这些变化也在易患阿尔茨海默病的转基因 C57BL/6 小鼠中观察到，这些小鼠对致病刺激有典型的神经退行性变反应。有趣的是，在仅感染线虫的小鼠中，更大的 M2 巨噬细胞群体导致强迫游泳测试的结果更好。鉴于神经退行性疾病负担不断增加，了解这种相互关联具有重要意义，可以为衰老健康策略和疾病监测提供参考。
