Related Experiment Video
Updated: Oct 27, 2025
Identifying Microglia and Peripheral Infiltrating Macrophages in the Injured Spinal Cords Using Flow Cytometry
Published on: June 24, 2025
Astrocyte-derived CCL7 promotes microglia-mediated inflammation following traumatic brain injury
Jianqin Xue1, Yu Zhang1, Junhua Zhang2
1Department of Rehabilitation Medicine, Jintan Hospital affiliated to Jiangsu University, Changzhou 213200, China.
Abstract:
Microglia are immune cells of the central nervous system that mediate neuroinflammation. It is widely known that microglia-mediated inflammation in the brain contribute to the widespread tissue damage and neurological deficits in traumatic brain injury (TBI). However, the mechanisms responsible for this inflammatory response remain elusive. Here, we investigated the role of astrocyte-derived chemokine (C-C motif) ligand 7 (CCL7) in microglial-controlled inflammation following TBI. Our results demonstrated that astrocyte-derived CCL7 induced microglial activation and the release of proinflammatory mediators in the cortex and serum of rats that underwent experimental TBI. Furthermore, CCL7 knockout improved microglia-controlled inflammation, brain morphology and neurological dysfunction following TBI. In vitro, CCL7-siRNA attenuated the LPS-induced expression of pro-inflammatory markers in the co-culture of microglia and astrocytes. Collectively, our findings uncover an important role for astrocyte-derived CCL7 in promoting microglia-mediated inflammation after TBI and suggests CCL7 could serve as a potential therapeutic strategy for attenuating TBI by inhibiting microglial activation.
Insights
Astrocyte-derived chemokine ligand 7 (CCL7) drives neuroinflammation after traumatic brain injury (TBI) by activating microglia. Inhibiting CCL7 may offer a therapeutic strategy for TBI by reducing microglial activation and improving outcomes.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Microglia are central nervous system immune cells mediating neuroinflammation.
- Microglia-driven inflammation exacerbates tissue damage and neurological deficits in traumatic brain injury (TBI).
- The precise mechanisms underlying TBI-induced neuroinflammation remain incompletely understood.
Purpose of the Study:
- To investigate the role of astrocyte-derived chemokine (C-C motif) ligand 7 (CCL7) in microglial-mediated inflammation following TBI.
- To elucidate the therapeutic potential of targeting CCL7 in TBI.
Main Methods:
- Experimental TBI induction in rats.
- CCL7 knockout rat model.
- In vitro co-culture of microglia and astrocytes with CCL7-siRNA.
- Analysis of inflammatory mediators in brain tissue and serum.
- Assessment of brain morphology and neurological function.
Main Results:
- Astrocyte-derived CCL7 significantly induced microglial activation and pro-inflammatory mediator release in TBI rats.
- CCL7 knockout ameliorated neuroinflammation, improved brain morphology, and enhanced neurological function post-TBI.
- In vitro, CCL7-siRNA reduced lipopolysaccharide (LPS)-induced pro-inflammatory marker expression in microglia-astrocyte co-cultures.
Conclusions:
- Astrocyte-derived CCL7 plays a critical role in promoting microglia-mediated inflammation after TBI.
- CCL7 inhibition represents a potential therapeutic target for mitigating TBI-induced neuroinflammation and neurological deficits.
