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CCL5 induces a pro-inflammatory profile in microglia in vitro
Jelena Skuljec1, Hui Sun, Refik Pul
1Department of Neurology, Hannover Medical School, Hannover, Germany.
Cellular Immunology
|May 31, 2011
Summary
Chemokines modulate microglia in neurodegenerative diseases. CCL5, a chemokine, not only attracts microglia but also alters their activated state by affecting nitric oxide and cytokine production.
Area of Science:
- Neuroscience
- Immunology
- Cell Biology
Background:
- Microglia express chemokine receptors (CCR1, CCR2, CCR3, CCR5, CXCR2) in neurodegenerative diseases like Alzheimer's and MS.
- Emerging evidence suggests chemokines may directly influence microglial reactivity beyond chemoattraction.
Purpose of the Study:
- To investigate the modulatory effects of specific chemokines (CCL2, CCL3, CCL5, CXCL1) on primary rat microglia.
- To determine the impact on cytokine production, nitric oxide (NO) synthesis, and phagocytosis.
Main Methods:
- Primary rat microglia were cultured and treated with CCL2, CCL3, CCL5, and CXCL1.
- Microglia were either non-stimulated or stimulated with lipopolysaccharide (LPS).
- Functional expression of receptors CCR1, CCR5, and CXCR2 was confirmed.
Main Results:
- All tested chemokines induced chemotaxis in microglia.
- CCL5 significantly increased nitric oxide (NO) secretion in activated microglia.
- CCL5 attenuated the production of IL-10 and IGF-1 in activated microglia.
Conclusions:
- Chemokine receptors CCR1, CCR5, and CXCR2 are functionally expressed on microglia.
- CCL5 exhibits a dual role, acting as a chemoattractant and modulating activated microglia profiles.
- These findings highlight CCL5's potential as a therapeutic target in neuroinflammation.
