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实验性抗磷脂综合征小鼠大脑中分泌的细胞因子水平发生显著变化。

Significant changes in the levels of secreted cytokines in brains of experimental antiphospholipid syndrome mice.

作者信息

Menachem Assaf, Chapman Joab, Katzav Aviva

机构信息

Department of Physiology and Pharmacology, Sackler Faculty of Medicine, Tel Aviv University, 69978 Tel Aviv, Israel.

出版信息

Autoimmune Dis. 2012;2012:404815. doi: 10.1155/2012/404815. Epub 2012 Feb 22.

DOI:10.1155/2012/404815
PMID:22454760
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3290816/
Abstract

Antiphospholipid syndrome (APS) is characterized by thromboses and neuropsychiatric manifestations possibly linked to brain inflammation. In order to examine the levels of proinflammatory and anti-inflammatory cytokines in experimental APS (eAPS) mice brains, we measured the levels of TNF-α, IFN-γ, and IL-10 in brain homogenates (cytosolic fractions) and in brain slices (secreted level) at 6, 15, and 24 weeks after immunization. We induced eAPS by immunization of Balb/c mice with β(2)-glycoprotein I (β(2)GPI), the major autoantigen in the disease and controls with adjuvant alone. We found increased levels of secreted TNF-α in eAPS mice for the entire experiment period. Cytosolic and secreted IL-10 and IFN-γ levels in eAPS mice were lower at 6 and 15 weeks and higher at 24 weeks after immunization. The results suggest that brain disease in APS is associated with significant and complex changes in proinflammatory and anti-inflammatory cytokines.

摘要

抗磷脂综合征（APS）的特征是血栓形成以及可能与脑部炎症相关的神经精神表现。为了检测实验性抗磷脂综合征（eAPS）小鼠大脑中促炎和抗炎细胞因子的水平，我们在免疫后6周、15周和24周测量了脑匀浆（胞质部分）和脑切片（分泌水平）中肿瘤坏死因子-α（TNF-α）、干扰素-γ（IFN-γ）和白细胞介素-10（IL-10）的水平。我们通过用β2糖蛋白I（β2GPI）免疫Balb/c小鼠诱导eAPS，β2GPI是该疾病的主要自身抗原，并单独用佐剂作为对照。我们发现，在整个实验期间，eAPS小鼠分泌的TNF-α水平升高。免疫后6周和15周，eAPS小鼠的胞质和分泌的IL-10以及IFN-γ水平较低，而在24周时较高。结果表明，APS中的脑部疾病与促炎和抗炎细胞因子的显著而复杂的变化有关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad29/3290816/8487ca33b3db/AD2012-404815.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad29/3290816/8fe327de209f/AD2012-404815.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad29/3290816/46676672c4f9/AD2012-404815.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad29/3290816/518ae269e64c/AD2012-404815.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad29/3290816/8487ca33b3db/AD2012-404815.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad29/3290816/8fe327de209f/AD2012-404815.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad29/3290816/46676672c4f9/AD2012-404815.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad29/3290816/518ae269e64c/AD2012-404815.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ad29/3290816/8487ca33b3db/AD2012-404815.004.jpg

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