Journal of Clinical Investigation · 2013 · 111 citations · 18 references
Life SciencesCardiologyImmunologyCell SignalingInflammationInnate ImmunityChronic InflammationCytokine BiologyInflammatory Cell ResponsesInflammatory MediatorsInflammatory SignalingMacrophage BiologyAtherosclerosis Molecular MechanismsAtherosclerosis-associated MacrophagesCholesterol EffluxChronic Inflammatory Disease ModelsFoam FormationInflammation In Cardiovascular DiseaseInflammatory ActivationPlaque Inflammation
The ELR(+)-CXCL chemokines have been described typically as potent chemoattractants and activators of neutrophils during the acute phase of inflammation. Their role in atherosclerosis, a chronic inflammatory vascular disease, has been largely unexplored. Using a mouse model of atherosclerosis, we found that CXCL5 expression was upregulated during disease progression, both locally and systemically, but was not associated with neutrophil infiltration. Unexpectedly, inhibition of CXCL5 was not beneficial but rather induced a significant macrophage foam cell accumulation in murine atherosclerotic plaques. Additionally, we demonstrated that CXCL5 modulated macrophage activation, increased expression of the cholesterol efflux regulatory protein ABCA1, and enhanced cholesterol efflux activity in macrophages. These findings reveal a protective role for CXCL5, in the context of atherosclerosis, centered on the regulation of macrophage foam cell formation.
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William A. Boisvert, Robert Santiago, Linda K. Curtiss et al. · Journal of Clinical Investigation · 1998 · 520 citations · Full text