Neutrophil activation is attenuated by high-density lipoprotein and apolipoprotein A-I in in vitro and in vivo models of inflammation.
Abstract
Objective—: Neutrophils play a key role in the immune response but can undesirably exacerbate inflammation. High-density lipoproteins (HDL) are antiinflammatory particles, exerting beneficial cardiovascular influences. We determined whether HDL exerts antiinflammatory effects on neutrophils and explored the mechanisms by which these occur. Methods and Results—: CD11b on activated human neutrophils was significantly attenuated by apolipoprotein A-I (apoA-I) and HDL. The effects of apoA-I were mediated via ABCA1, whereas the effects of HDL were via scavenger receptor BI. Both were associated with a reduction in the abundance of lipid rafts, and a strong correlation between raft abundance and CD11b activation was observed. ApoA-I and HDL reduced neutrophil adhesion to a platelet monolayer under shear flow, as well as neutrophil spreading and migration. ApoA-I also inhibited leukocyte recruitment to the endothelium in an acute in vivo model of inflammation. Finally, infusion of reconstituted HDL in patients with peripheral vascular disease was demonstrated to significantly attenuate neutrophil activation. Conclusion—: We describe here a novel role for HDL and apoA-I in regulating neutrophil activation using in vitro, in vivo, and clinical approaches. We also show that these effects of HDL and apoA-I involve a mechanism requiring changes in membrane domain content rather than in cholesterol efflux per se.
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HDL inhibits the activation, attachment, diffusion, and migration of neutrophils and the activities of monocytes.
“HDL has been found to inhibit the activation, attachment, diffusion, and migration of neutrophils (43) and the activities of monocytes (48).”
From Investigation of systemic immune-inflammation index, neutrophil/high-density lipoprotein ratio, lymphocyte/high-density lipoprotein ratio, and monocyte/high-density lipoprotein ratio as indicators of inflammation in patients with schizophrenia and bipolar disorder (2022) · cites this paper as [43]
HDL-C suppresses neutrophil activation, adhesion, proliferation, and migration.
“Conversely, HDL-C suppresses neutrophil activation, adhesion, proliferation, and migration (23).”
From Retrospective evaluation of novel serum inflammatory biomarkers in first-episode psychiatric disorders: diagnostic potential and immune dysregulation (2024) · cites this paper as [23]
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- Authors
- Murphy, A. J., Woollard, K. J., Suhartoyo, A., Stirzaker, R. A., Shaw, J., Sviridov, D., & Chin-Dusting, J. P. F.
- Affiliations
- Baker Heart and Diabetes Institute (AU)
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2011-06
- Volume
- 31
- Issue
- 6
- Pages
- 1333-1341
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W2125808969
- Cited by
- 244
- References
- 34
- Citations by year
- 2026: 17 · 2025: 23 · 2024: 23 · 2023: 28 · 2022: 14 · 2021: 28 · 2020: 16 · 2019: 16 · 2018: 4 · 2017: 8 · 2016: 9 · 2015: 8 · 2014: 17 · 2013: 18 · 2012: 11
- FWCI
- 16.35
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Arteriosclerosis Thrombosis and Vascular Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Medical Research Council
- National Health and Medical Research Council
- Topics
- Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
- Keywords
- high-density lipoprotein, apolipoprotein A-I, neutrophil activation, inflammation, CD11b, ABCA1, scavenger receptor BI, lipid rafts, neutrophil adhesion, neutrophil migration, leukocyte recruitment, peripheral vascular disease
- MeSH terms
- Animals, Cell Adhesion, Cell Movement, Cholesterol, Humans, Inflammation, Lipoproteins, HDL, Male, Mice, Inbred C57BL, Tetradecanoylphorbol Acetate, Peripheral Vascular Diseases, Apolipoprotein A-I, Neutrophil Activation, Membrane Microdomains, CD11b Antigen, Scavenger Receptors, Class B, Mice
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