Aβ-induced Phagocytosis and Inflammation Assay Service
Our Aβ-induced phagocytosis and inflammation assay service is widely used in various research fields, such as drug development and pathological mechanisms, to screen potential therapeutic targets and provide new insights into the pathogenesis of Alzheimer's disease (AD). For further information regarding the products and services provided, project-specific consultation, and pricing, please submit an inquiry here.
Introduction
One of the pathological hallmarks of AD is the excessive accumulation of amyloid beta peptide (Aβ). Aβ triggers a series of inflammatory responses by interacting with immune cells such as astrocytes and microglia, leading to neuronal damage and cognitive decline. Microglia, as the main immune cells of the central nervous system, are responsible for clearing Aβ plaques, but their dysfunction in AD leads to decreased clearance efficiency and the release of more inflammatory factors. In addition, Aβ-induced phagocytosis also be mediated by receptors such as TREM2 and CD36, further influencing the occurrence of neuroinflammation.
Aβ-induced Phagocytosis and Inflammation Assay
Our testing services focus on Aβ-induced phagocytosis and the associated inflammatory response, using advanced flow cytometry, fluorescence microscopy and biomarker analysis to accurately assess the following aspects:
- Aβ Phagocytosis Efficiency Assay
Flow cytometry was used to detect the uptake of Aβ by specific cell lines (such as HMC3, N9, etc.), and the phagocytosis process was observed in combination with fluorescence labeling technology. At the same time, we can further distinguish between non-specific phagocytosis and specific phagocytosis. Through TAM receptor-dependent phagocytosis mediated by targeted antibodies, Aβ can be cleared more precisely without inducing an inflammatory response.
Fig.1 BV2 and primary microglial phagocytosis.2
By analyzing inflammatory mediators in the cell culture supernatant and correlating them with microglial phagocytosis, specific phagocytosis can be distinguished from non-specific phagocytosis.
Fig.2 Correlations between inflammatory mediators and the phagocytic response.2
- Inflammatory Factor Assay
ELISA: The ELISA method can be used to quantitatively detect the levels of inflammatory factors (such as IL-1β, TNF-α, IL-6, etc.) to evaluate the inflammatory response induced by Aβ.
PCR and Western blot: These molecular biology techniques can be used to detect changes in the expression of inflammation-related genes and proteins, such as key proteins in the NF-κB pathway.
- Analysis of Microglial Phenotype
Under Aβ stimulation, microglia change from a quiescent state to an activated state and show significant morphological changes. Combined with our high-content imaging (HCI) analysis platform, we can analyze the phenotypic changes of microglia at different stages under Aβ stimulation.
Fig.3 Microglial polarization induced by inflammatory factors and Aβ.3
Please contact us for more information about our Aβ-induced phagocytosis and inflammation assay services. We look forward to working with you to advance research in neurodegenerative diseases!
References
- Sun, Zhongqing, et al. "Targeting Microglia in Alzheimer's Disease: Pathogenesis and Potential Therapeutic Strategies." Biomolecules 14.7 (2024): 833. Distributed under Open Access license CC BY 4.0, without modification.
- Pan, Xiao-dong, et al. "Microglial phagocytosis induced by fibrillar β-amyloid is attenuated by oligomeric β-amyloid: implications for Alzheimer's disease." Molecular neurodegeneration 6 (2011): 1-18. Distributed under Open Access license CC BY 2.0, without modification.
- Xie, Lushuang, et al. "Inflammatory factors and amyloid β-induced microglial polarization promote inflammatory crosstalk with astrocytes." Aging (Albany NY) 12.22 (2020): 22538. Distributed under Open Access license CC BY 3.0, without modification.
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