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|Title: ||Low-density lipoprotein receptor deficiency attenuates neuroinflammation through the induction of apolipoprotein|
|Authors: ||Mailleux, Jo|
Van Horssen, Jack
Bogie, Jeroen F. J.
Hendriks, Jerome J. A.
|Issue Date: ||2017|
|Citation: ||Frontiers in Immunology, 8, p. 1-12 (Art N° 1701)|
|Abstract: ||Objective: We aimed to determine the role of the low-density lipoprotein receptor (LDLr) in neuroinflammation by inducing experimental autoimmune encephalomyelitis (EAE) in ldlr knock out mice. Methods: MOG35–55 induced EAE in male and female ldlr−/− mice was assessed clinically and histopathologically. Expression of inflammatory mediators and apolipoprotein E (apoE) was investigated by qPCR. Changes in protein levels of apoE and tumor necrosis
factor alpha (TNFα) were validated by western blot and ELISA, respectively.
results: Ldlr−/−-attenuated EAE disease severity in female, but not in male, EAE mice marked by a reduced proinflammatory cytokine production in the central nervous system of female ldlr−/− mice. Macrophages from female ldlr−/− mice showed a similar decrease in
proinflammatory mediators, an impaired capacity to phagocytose myelin and enhanced secretion of the anti-inflammatory apoE. Interestingly, apoE/ldlr double knock out abrogated the beneficial effect of ldlr depletion in EAE.
conclusion: Collectively, we show that ldlr−/− reduces EAE disease severity in female but not in male EAE mice, and that this can be explained by increased levels of apoE in female ldlr−/− mice. Although the reason for the observed sexual dimorphism remains
unclear, our findings show that LDLr and associated apoE levels are involved in neuroinflammatory processes.|
|ISI #: ||000416523900001|
|Type: ||Journal Contribution|
|Appears in Collections: ||Research publications|
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