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Updated: May 5, 2026

Culture of Macrophage Colony-stimulating Factor Differentiated Human Monocyte-derived Macrophages
Published on: June 30, 2016
CXCL5 limits macrophage foam cell formation in atherosclerosis
Anthony Rousselle1, Fatimunnisa Qadri, Lisa Leukel
1Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Chemokines like CXCL5, typically linked to acute inflammation, surprisingly protect against atherosclerosis. This study reveals CXCL5
Area of Science:
- Immunology
- Cardiovascular Research
- Molecular Biology
Background:
- ELR(+) CXCL chemokines are known neutrophil chemoattractants in acute inflammation.
- The function of these chemokines in chronic inflammatory diseases like atherosclerosis is largely unknown.
Purpose of the Study:
- To investigate the role of CXCL5 in atherosclerosis.
- To understand the mechanisms underlying CXCL5's function in this disease context.
Main Methods:
- Utilized a mouse model of atherosclerosis.
- Analyzed CXCL5 expression during disease progression.
- Investigated the effects of CXCL5 inhibition on plaque development.
- Examined CXCL5's impact on macrophage activation and cholesterol metabolism.
Main Results:
- CXCL5 expression increased with atherosclerosis progression, independent of neutrophil infiltration.
- Inhibiting CXCL5 exacerbated plaque formation by promoting macrophage foam cell accumulation.
- CXCL5 was found to modulate macrophage activation and enhance cholesterol efflux via ABCA1.
Conclusions:
- CXCL5 plays a protective role in atherosclerosis by regulating macrophage foam cell formation.
- The findings challenge the traditional view of CXCL chemokines and highlight a novel therapeutic target for atherosclerosis.
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