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CD36 mediates the innate host response to beta-amyloid
Joseph B El Khoury1, Kathryn J Moore, Terry K Means
1Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy and Immunology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.
Abstract:
Accumulation of inflammatory microglia in Alzheimer's senile plaques is a hallmark of the innate response to beta-amyloid fibrils and can initiate and propagate neurodegeneration characteristic of Alzheimer's disease (AD). The molecular mechanism whereby fibrillar beta-amyloid activates the inflammatory response has not been elucidated. CD36, a class B scavenger receptor, is expressed on microglia in normal and AD brains and binds to beta-amyloid fibrils in vitro. We report here that microglia and macrophages, isolated from CD36 null mice, had marked reductions in fibrillar beta-amyloid-induced secretion of cytokines, chemokines, and reactive oxygen species. Intraperitoneal and stereotaxic intracerebral injection of fibrillar beta-amyloid in CD36 null mice induced significantly less macrophage and microglial recruitment into the peritoneum and brain, respectively, than in wild-type mice. Our data reveal that CD36, a major pattern recognition receptor, mediates microglial and macrophage response to beta-amyloid, and imply that CD36 plays a key role in the proinflammatory events associated with AD.
Insights
CD36, a receptor on immune cells, triggers inflammation in Alzheimer's disease (AD) by binding to beta-amyloid. Blocking CD36 reduces inflammatory responses and cell recruitment in AD models.
Area of Science:
- Neuroscience
- Immunology
- Alzheimer's Disease Research
Background:
- Microglia activation and inflammation are central to Alzheimer's disease (AD) pathogenesis.
- Beta-amyloid fibrils are known triggers of this inflammatory response.
- The precise molecular mechanisms linking beta-amyloid to microglial activation remain unclear.
Purpose of the Study:
- To elucidate the molecular mechanisms of fibrillar beta-amyloid-induced inflammatory response in microglia.
- To investigate the role of CD36, a scavenger receptor, in mediating microglial and macrophage activation by beta-amyloid.
Main Methods:
- Utilized CD36 null mice and wild-type littermates.
- Isolated microglia and macrophages for in vitro stimulation with fibrillar beta-amyloid.
- Assessed cytokine, chemokine, and reactive oxygen species secretion.
- Evaluated inflammatory cell recruitment in vivo following beta-amyloid administration.
Main Results:
- Microglia and macrophages from CD36 null mice showed significantly reduced inflammatory mediator secretion upon beta-amyloid exposure.
- CD36 null mice exhibited markedly decreased recruitment of macrophages and microglia to sites of beta-amyloid injection.
- CD36 was identified as a key mediator of the innate immune response to beta-amyloid.
Conclusions:
- CD36 acts as a crucial pattern recognition receptor mediating the inflammatory response of microglia and macrophages to beta-amyloid.
- CD36 plays a significant role in the pro-inflammatory events contributing to Alzheimer's disease.
- Targeting CD36 may offer a therapeutic strategy for mitigating neuroinflammation in AD.
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