Evidence map›Paper›PMID 12228258›Full record

ArticleInfection and immunity2002

The class A macrophage scavenger receptor is a major pattern recognition receptor for Neisseria meningitidis which is independent of lipopolysaccharide and not required for secretory responses.

Leanne Peiser, Menno P J De Winther, Katherine Makepeace, Michael Hollinshead, Philip Coull, Joyce Plested, Tatsuhiko Kodama, E Richard Moxon, Siamon Gordon

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

52 citing papers in PubMed, 141 citations in OpenAlex.

  1. PostbioticFrontiers in immunology · 2026
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  4. The Host-Pathogen Interactions and Epicellular Lifestyle ofFrontiers in cellular and infection microbiology · 2022
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  5. Article
  6. Scavenger receptor A1 participates in uptake ofEmerging microbes & infections · 2021
    Article
  7. Article
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  9. Article
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  13. Article
  14. Article
  15. CD163Scientific reports · 2017
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

9 authors at 4 institutions in 3 countries.

Leanne PeiserSir William Dunn School of Pathology, Oxford University, Oxford, United Kingdom.
Menno P J De Winther
Katherine Makepeace
Michael Hollinshead
Philip Coull
Joyce Plested
Tatsuhiko Kodama
E Richard Moxon
Siamon Gordon
University of Oxford · GBJohn Radcliffe Hospital · GBMaastricht University · NLThe University of Tokyo · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophages (Mphi) play a key role in the pathogenesis of invasive meningococcal infections. The roles of two pattern recognition molecules, the Mphi scavenger receptor (SR-A) and Toll-like receptor 4 (TLR-4), have been investigated using bone marrow culture-derived Mphi (BMMphi). Surprisingly, a comparison of BMMphi from wild-type and SR-A knockout (SR-A(-/-)) mice showed that nonopsonic phagocytosis of meningococci was mediated almost exclusively via SR-A. Previous studies have demonstrated only a partial involvement of the receptor in the uptake of other bacteria, such as Escherichia coli. Interestingly, we also show that lipopolysaccharide (LPS) was not the ligand for the receptor on these organisms. Further study of the downstream events of SR-A-mediated ingestion of Neisseria meningitidis demonstrated that SR-A was not required for cytokine production. To determine the bacterial and host factors required to stimulate Mphi activation, we examined TLR-4-deficient Mphi from C3H/HeJ mice and LPS-deficient meningococci. TLR-4-deficient cells elaborated reduced amounts of tumor necrosis factor alpha, interleukin-12 (IL-12), and IL-10, even though ingestion via SR-A was unaffected in these cells. Similarly, although there was no change in SR-A-mediated ingestion of LPS-deficient meningococci, the mutant failed to stimulate a Mphi-dependent cytokine response. Thus, we show that Mphi SR-A mediates opsonin-independent uptake of N. meningitidis independently of lipid A and that this activity is uncoupled from the Mphi secretion of proinflammatory cytokines, which provides a basis for further investigation of the role of this receptor in meningococcal disease in humans.

Indexed as

Drosophila ProteinsAnimalsCytokinesLipid AMacrophage ActivationMacrophagesMembrane GlycoproteinsMeningococcal InfectionsMiceMice, Inbred C3HMice, KnockoutMicroscopy, ElectronNeisseria meningitidisPhagocytosisPhagosomesReceptors, Cell SurfaceCytokinesDrosophila ProteinsLipid AMembrane GlycoproteinsMsr1 protein, mouseReceptors, Cell SurfaceReceptors, ImmunologicReceptors, ScavengerScavenger Receptors, Class AToll-Like Receptor 4Toll-Like Receptors

Identifiers

PMID12228258
PMCPMC128305
OpenAlexW2079013718

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.