Inflammatory Chemokines Expression Variations and Their Receptors in APP/PS1 Mice

CCR3 趋化因子 CCR1 炎症 CCR10 CCL13型 趋化因子受体 免疫学 CCL7型 CCL11型 早老素 受体 生物 CCR2型 CXCL2型 淀粉样前体蛋白 阿尔茨海默病 四氯化碳 医学 内科学 疾病 生物化学
作者
Adrián Jordá,Martı́n Aldasoro,Constanza Aldasoro,Soraya L. Vallés
出处
期刊:Journal of Alzheimer's Disease [IOS Press]
卷期号:83 (3): 1051-1060 被引量:7
标识
DOI:10.3233/jad-210489
摘要

In Alzheimer's disease (AD), an increase in inflammation is distinctive. Amyloid precursor protein plus presenilin-1 (APP/PS1 mice) is a model for this illness. Chemokines secreted by central nervous system (CNS) cells could play multiple important roles in AD. Data looking for the chemokines involved in inflammatory mechanisms are lacking. To understand the changes that occur in the inflammation process in AD, it is necessary to improve strategies to act on specific inflammatory targets.Chemokines and their receptors involved in phagocytosis, demyelination, chemotaxis, and coagulation were the objective of our study.Female APPswe/PS1 double-transgenic mice (B6C3-Tg) were used and cortex brain from 20-22-month-old mice obtained and used to quantify chemokines and chemokine receptors expression using RT-PCR technique.Significant inflammatory changes were detected in APP/PS1 compared to wild type mice. CCR1, CCR3, CCR4, and CCR9 were elevated, and CCR2 were decreased compared with wild type mice. Their ligands CCL7, CCL11, CCL17, CCL22, CCL25, and CXCL4 showed an increase expression; however, changes were not observed in CCL2 in APP/PS1 compared to wild type mice.This change in expression could explain the differences between AD patients and elderly people without this illness. This would provide a new strategy for the treatment of AD, with the possibility to act in specific inflammatory targets.
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