Evidence map›Paper›PMID 34663245›Full record

ArticleBMC infectious diseases2021

IL-18 and IL-18 binding protein are related to disease severity and parasitemia during falciparum malaria.

Kari Otterdal, Aase Berg, Annika E Michelsen, Arne Yndestad, Sam Patel, Ida Gregersen, Bente Halvorsen, Thor Ueland, Nina Langeland, Pål Aukrust

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC infectious diseases, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 2 pooled it
0.7field-weighted citation impact, top 30% 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

8 citing papers in PubMed, 2 syntheses or guidelines pooled it, 11 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. Review
  5. Article
  6. Review
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  8. Review
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

10 authors at 6 institutions in 4 countries.

Kari OtterdalResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Nydalen, PO Box 4950, 0424, Oslo, Norway. kari.otterdal@ous-research.no.
Aase BergDepartment of Medicine, Stavanger University Hospital, PO Box 8100, 4068, Stavanger, Norway.
Annika E MichelsenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Nydalen, PO Box 4950, 0424, Oslo, Norway.
Arne YndestadResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Nydalen, PO Box 4950, 0424, Oslo, Norway.
Sam PatelDepartment of Medicine, Central Hospital of Maputo, Maputo, Mozambique.
Ida GregersenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Nydalen, PO Box 4950, 0424, Oslo, Norway.
Bente HalvorsenResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Nydalen, PO Box 4950, 0424, Oslo, Norway.
Thor UelandResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Nydalen, PO Box 4950, 0424, Oslo, Norway.
Nina LangelandDepartment of Clinical Science, University of Bergen, 5021, Bergen, Norway.
Pål AukrustResearch Institute of Internal Medicine, Oslo University Hospital Rikshospitalet, Nydalen, PO Box 4950, 0424, Oslo, Norway.
Oslo University Hospital · NOUniversity of Oslo · NOHaukeland University Hospital · NOMaputo Central Hospital · MZStavanger University Hospital · NOThrombosis Research Institute · GB

Funding

Helse Sør-Øst RHF 2015060Helse Vest 911539
6 · The paper itself

Abstract

backgroundSeveral inflammatory molecules participate in the immune response to malaria. Interleukin (IL)-18 is an inflammatory cytokine activated by NLRP3 inflammasomes. In clinical falciparum malaria, with and without HIV co-infection, data on IL-18 and in particular on its binding protein, IL-18bp, is scarce.

methodsClinical data and blood samples were collected from adults in Mozambique with P. falciparum infection, with (n = 70) and without (n = 61) HIV co-infection, from HIV-infected patients with similar symptoms without malaria (n = 58) and from healthy controls (n = 52). In vitro studies were performed in endothelial cells using hemozoin crystals.

results(i) IL-18 and IL-18bp were markedly up-regulated during falciparum malaria with particular high levels in malaria patients co-infected with HIV and severe malaria disease. (ii) In the malaria group as a whole, both IL-18 and IL-18bp were positively correlated with disease severity, parasitemia, and endothelial cell activation as assessed by vWF in plasma. (iii) Whereas there was no change in IL-18 levels in malaria patients co-infected with HIV during follow-up, the patients with malaria only had slightly increased IL-18 levels. Further, the IL-18pb levels declined and thereby contributed to an increase in IL-18/IL-18bp ratio in all subgroups of malaria patients. (iv) IL-27, previously shown to be up-regulated in this malaria cohort, markedly induced a release of IL-18bp from endothelial cells in vitro, and notably, this presumably anti-inflammatory effect was counteracted by hemozoin.

conclusionsOur findings suggest that the IL-18 system could be an important mediator in the immune pathogenesis during falciparum malaria, potentially also representing a target for therapy.

Indexed as

Interleukin-18MalariaEndothelial CellsHumansIntercellular Signaling Peptides and ProteinsParasitemiaSeverity of Illness IndexIntercellular Signaling Peptides and ProteinsInterleukin-18interleukin-18 binding proteinEndothelial cellsFalciparum malariaHIVIL-18IL-18bp

Identifiers

PMID34663245
PMCPMC8524870
OpenAlexW3207313053

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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.