The DOI matches its Crossref record; 34 of the 34 references it cites were found in a registry or an index.
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.
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The cited source says what the claim attributes to it.
In the citing paper
“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]
In the citing paper
“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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
Cites
High-Density Lipoproteins Inhibit Cytokine-Induced Expression of Endothelial Cell Adhesion Molecules
COCKERILL, G. W., Rye, K., Gamble, J. R., Vadas, M. A., & Barter, P. J. (1995) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/01.atv.15.11.1987 · Cited by 788
ATP-Binding Cassette Transporters and HDL Suppress Hematopoietic Stem Cell Proliferation
Yvan‐Charvet, L., Pagler, T. A., Gautier, E. L., Avagyan, S., Siry, R., Han, S., Welch, C. L., Wang, N., Randolph, G. J., Snoeck, H. W., et al. (2010) · Science · doi:10.1126/science.1189731 · Cited by 724
Hyperlipidemia-triggered neutrophilia promotes early atherosclerosis
Drechsler, M., Megens, R. T. A., van Zandvoort, M., Weber, C., & Soehnlein, O. (2010) · Circulation · doi:10.1161/circulationaha.110.961714 · Cited by 698
High-Density Lipoprotein Reduces the Human Monocyte Inflammatory Response
Murphy, A. J., Woollard, K. J., Hoang, A., Mukhamedova, N., Stirzaker, R. A., McCormick, S. P. A., Remaley, A. T., Sviridov, D., & Chin-Dusting, J. P. F. (2008) · Arteriosclerosis Thrombosis and Vascular Biology · doi:10.1161/atvbaha.108.168690 · Cited by 511
Self-citationYvan-Charvet, L., Welch, C., Pagler, T. A., Ranalletta, M., Lamkanfi, M., Han, S., Ishibashi, M., Li, R., Wang, N., & Tall, A. R. (2008) · Circulation · doi:10.1161/circulationaha.108.793869 · Cited by 439
Zernecke, A., Bot, I., Djalali-Talab, Y., Shagdarsuren, E., Bidzhekov, K., Meiler, S. U., Krohn, R. M., Schober, A., Sperandio, M., Soehnlein, O., et al. (2007) · Circulation Research · doi:10.1161/circresaha.107.160697 · Cited by 414
Apolipoprotein Specificity for Lipid Efflux by the Human ABCAI Transporter
Remaley, A. T., Stonik, J. A., Demosky, S. J., Neufeld, E. B., Bocharov, A. V., Vishnyakova, T. G., Eggerman, T. L., Patterson, A. P., Duverger, N., Santamarina-Fojo, S., et al. (2001) · Biochemical and Biophysical Research Communications · doi:10.1006/bbrc.2000.4219 · Cited by 327
Mechanisms underlying neutrophil-mediated monocyte recruitment
Soehnlein, O., Lindbom, L., & Weber, C. (2009) · Blood · doi:10.1182/blood-2009-06-221630 · Cited by 312
Yancey, P. G., de la Llera-Moya, M., Swarnakar, S., Monzo, P., Klein, S. M., Connelly, M. A., Johnson, W. J., Williams, D. L., & Rothblat, G. H. (2000) · Journal of Biological Chemistry · doi:10.1074/jbc.m006924200 · Cited by 312
Shaw, J. A., Bobik, A., Murphy, A. J., Kanellakis, P., Blombery, P. A., Mukhamedova, N., Woollard, K. J., Lyon, S. M., Sviridov, D., & Dart, A. M. (2008) · Circulation Research · doi:10.1161/circresaha.108.182063 · Cited by 280
Self-citation
Cited by
Sorted by citations
Murphy, A. J., Akhtari, M., Tolani, S., Pagler, T., Bijl, N., Kuo, C.-L., Wang, M., Sanson, M., Abramowicz, S., Welch, C., et al. (2011) · Journal of Clinical Investigation · doi:10.1172/jci57559 · Cited by 521
Self-citationMultiple Roles for Neutrophils in Atherosclerosis
Soehnlein, O. (2012) · Circulation Research · doi:10.1161/circresaha.111.257535 · Cited by 514
Molecular Biology of Atherosclerosis
Hopkins, P. N. (2013) · Physiological Reviews · doi:10.1152/physrev.00004.2012 · Cited by 467
HDL in innate and adaptive immunity
Catapano, A. L., Pirillo, A., Bonacina, F., & Norata, G. D. (2014) · Cardiovascular Research · doi:10.1093/cvr/cvu150 · Cited by 301
ATP-Binding Cassette Transporters, Atherosclerosis, and Inflammation
Westerterp, M., Bochem, A. E., Yvan‐Charvet, L., Murphy, A. J., Wang, N., & Tall, A. R. (2014) · Circulation Research · doi:10.1161/circresaha.114.300738 · Cited by 261
Self-citation
Metadata
- 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
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Cholesterol and Lipid Metabolism
- Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › 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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
