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In vitro Quantitative Imaging Assay for Phagocytosis of Dead Neuroblastoma Cells by iPSC-Macrophages

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Impact Induces Phagocytic Defect in Reactive Microglia.

Ruilin Yu¹, Edmond A Rogers^2,3,4, Palak Manchanda¹

¹Department of Chemistry, Purdue University, West Lafayette, IN 47907, USA.

Biorxiv : the Preprint Server for Biology

|September 26, 2025

Summary

This summary is machine-generated.

This study introduces a traumatic brain injury (TBI) chip model. The TBI chip reveals reduced microglial phagocytosis and impaired neuronal function, alongside altered lipid metabolism, offering insights into neuroinflammation and neurodegeneration.

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Area of Science:

Neuroscience
Biotechnology
Cell Biology

Background:

Traumatic brain injury (TBI) poses significant challenges in understanding neuroinflammation and neurodegeneration.
In vitro models are crucial for studying cellular responses to TBI.
Lipid metabolism is implicated in brain trauma and neurodegenerative diseases.

Purpose of the Study:

To develop and utilize a TBI-on-a-chip model to investigate molecular and cellular changes post-impact.
To assess the impact of TBI on microglial phagocytosis and neuronal function.
To analyze alterations in the cellular lipidome following TBI.

Main Methods:

Development of a TBI-on-a-chip model using primary microglia and neuronal networks.
Utilized a pH-responsive amyloid β (AβpH) assay to measure microglial phagocytosis.
Electrophysiological recordings to assess neuronal firing frequency.
Lipidomic analysis of secreted lipids from impacted cells.

Main Results:

Microglial phagocytosis was significantly reduced at 7 days post-impact in the TBI chip model.
Neurons exhibited increased amyloid β uptake and decreased firing frequency at 7 days post-impact.
Significant alterations were observed in lipid species from sphingomyelin, glycerophospholipid, and phosphatidylserine classes.

Conclusions:

The TBI-on-a-chip model effectively recapitulates key cellular and molecular changes following brain injury.
Impaired microglial function and neuronal activity, coupled with altered lipid metabolism, are critical consequences of TBI.
These findings highlight the role of lipid metabolism in neuroinflammation resolution and neurodegeneration pathogenesis after TBI.