期刊
FRONTIERS IN NEUROLOGY
卷 12, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fneur.2021.629332
关键词
neuroinflammation; chitinases; macrophages; neurodegeneration; ageing
资金
- German Bundesministerium fur Bildung und Forschung (BMBF) grant SOPHIA under the EU Joint Programme Neurodegenerative Disease Research (JPND)
- German Bundesministerium fur Bildung und Forschung (BMBF) grant ONWebDUALS under the EU Joint Programme Neurodegenerative Disease Research (JPND)
- BMBF grant PYRAMID
- Bundesministerium fur Bildung und Forschung [01GY1804]
- Motor Neurone Disease Association (MNDA)
- Deutsche Gesellschaft fur Muskelkranke (DGM)
- Deutsche Forschungsgemeinschaft (DFG)
- Graduate Academy of Friedrich Schiller University, Jena, Germany
- state of Thuringia
- German Research Foundation
- Thueringer Universitaets-und Landesbibliothek Jena [433052568]
The study found that immune cells in ALS patients have an inherently increased potential for chitinase production, which may contribute to chronic neuroinflammation, and that age influences the levels of CHI3L1.
Neuroinflammation significantly contributes to Amyotrophic Lateral Sclerosis (ALS) pathology. In lieu of this, reports of elevated chitinase levels in ALS are interesting, as they are established surrogate markers of a chronic inflammatory response. While post-mortem studies have indicated glial expression, the cellular sources for these moieties remain to be fully understood. Therefore, the objective of this pilot study was to examine whether the peripheral immune system also contributes to chitinase dysregulation in ALS. The temporal expression of CHIT1, CHI3L1, and CHI3L2 in non-polarized monocyte-derived macrophages (MoMas) from ALS patients and healthy controls (HCs) was examined. We demonstrate that while CHIT1 and CHI3L1 display similar temporal expression dynamics in both groups, profound between-group differences were noted for these targets at later time-points i.e., when cells were fully differentiated. CHIT1 and CHI3L1 expression were significantly higher in MoMas from ALS patients at both the transcriptomic and protein level, with CHI3L1 levels also being influenced by age. Conversely, CHI3L2 expression was not influenced by disease state, culture duration, or age. Here, we demonstrate for the first time, that in ALS, circulating immune cells have an intrinsically augmented potential for chitinase production that may propagate chronic neuroinflammation, and how the ageing immune system itself contributes to neurodegeneration.
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