Evidence map›Paper›PMID 30519244›Full record

ArticleFrontiers in immunology2018

Complement Factor H and Apolipoprotein E Participate in Regulation of Inflammation in THP-1 Macrophages.

Eija Nissilä, Pipsa Hakala, Katarzyna Leskinen, Angela Roig, Shahan Syed, Kok P M Van Kessel, Jari Metso, Carla J C De Haas, Päivi Saavalainen, Seppo Meri and 6 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.6field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Exploring the intersection of atherosclerosis and Alzheimer's disease: the role of inflammation and complement activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  4. Article
  5. Article
  6. Article
  7. Review
  8. The human factor H protein family - an update.Frontiers in immunology · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Review
  16. Apolipoprotein E and Atherosclerosis.Current atherosclerosis reports · 2021
    Review
  17. Observational
  18. Article
  19. Article
  20. Apolipoprotein E in Asthmatic Inflammatory Response: Friend or Foe?American journal of respiratory cell and molecular biology · 2020
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 5 institutions in 3 countries.

Eija NissiläDepartment of Bacteriology and Immunology, and Research Programs Unit, Immunobiology, University of Helsinki, Helsinki, Finland.
Pipsa HakalaDepartment of Bacteriology and Immunology, and Research Programs Unit, Immunobiology, University of Helsinki, Helsinki, Finland.
Katarzyna LeskinenDepartment of Bacteriology and Immunology, and Research Programs Unit, Immunobiology, University of Helsinki, Helsinki, Finland.
Angela RoigDepartment of Bacteriology and Immunology, and Research Programs Unit, Immunobiology, University of Helsinki, Helsinki, Finland.
Shahan SyedDepartment of Bacteriology and Immunology, and Research Programs Unit, Immunobiology, University of Helsinki, Helsinki, Finland.
Kok P M Van KesselMedical Microbiology, University Medical Center Utrecht, Utrecht, Netherlands.
Jari MetsoMinerva Foundation Institute for Medical Research, Helsinki, Finland.
Carla J C De HaasMedical Microbiology, University Medical Center Utrecht, Utrecht, Netherlands.
Päivi SaavalainenDepartment of Bacteriology and Immunology, and Research Programs Unit, Immunobiology, University of Helsinki, Helsinki, Finland.
Seppo MeriDepartment of Bacteriology and Immunology, and Research Programs Unit, Immunobiology, University of Helsinki, Helsinki, Finland.
Angeliki ChroniInstitute of Biosciences and Applications, National Center for Scientific Research "Demokritos", Athens, Greece.
Jos A G Van StrijpMedical Microbiology, University Medical Center Utrecht, Utrecht, Netherlands.
Katariina ÖörniWihuri Research Institute, Helsinki, Finland.
Matti JauhiainenMinerva Foundation Institute for Medical Research, Helsinki, Finland.
T Sakari JokirantaDepartment of Bacteriology and Immunology, and Research Programs Unit, Immunobiology, University of Helsinki, Helsinki, Finland.
Karita HaapasaloDepartment of Bacteriology and Immunology, and Research Programs Unit, Immunobiology, University of Helsinki, Helsinki, Finland.
University of Helsinki · FIUniversity Medical Center Utrecht · NLMinerva Foundation · FINational Centre of Scientific Research "Demokritos" · GRWihuri Research Institute · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The alternative pathway (AP) of complement is constantly active in plasma and can easily be activated on self surfaces and trigger local inflammation. Host cells are protected from AP attack by Factor H (FH), the main AP regulator in plasma. Although complement is known to play a role in atherosclerosis, the mechanisms of its contribution are not fully understood. Since FH via its domains 5-7 binds apoliporotein E (apoE) and macrophages produce apoE we examined how FH could be involved in the antiatherogenic effects of apoE. We used blood peripheral monocytes and THP-1 monocyte/macrophage cells which were also loaded with acetylated low-density lipoprotein (LDL) to form foam cells. Binding of FH and apoE on these cells was analyzed by flow cytometry. High-density lipoprotein (HDL)-mediated cholesterol efflux of activated THP-1 cells was measured and transcriptomes of THP-1 cells using mRNA sequencing were determined. We found that binding of FH to human blood monocytes and cholesterol-loaded THP-1 macrophages increased apoE binding to these cells. Preincubation of fluorescent cholesterol labeled THP-1 macrophages in the presence of FH increased cholesterol efflux and cholesterol-loaded macrophages displayed reduced transcription of proinflammatory/proatherogenic factors and increased transcription of anti-inflammatory/anti-atherogenic factors. Further incubation of THP-1 cells with serum reduced C3b/iC3b deposition. Overall, our data indicate that apoE and FH interact with monocytic cells in a concerted action and this interaction reduces complement activation and inflammation in the atherosclerotic lesions. By this way FH may participate in mediating the beneficial effects of apoE in suppressing atherosclerotic lesion progression.

Indexed as

Apolipoproteins EAtherosclerosisComplement C3bComplement Factor HFoam CellsHumansInflammationLipoproteins, HDLMonocytesTHP-1 CellsTranscription, GeneticApoE protein, humanApolipoproteins EComplement C3bComplement Factor HLipoproteins, HDLapolipoprotein Eatherosclerosiscomplementcomplement systemFactor Hinflammation

Identifiers

PMID30519244
PMCPMC6260146
OpenAlexW2900899382

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.