Evidence map›Paper›PMID 39062668›Full record

ArticleGenes2024

Pathway-Based Mendelian Randomization for Pre-Infection IL-6 Levels Highlights Its Role in Coronavirus Disease.

Zoha Kamali, Nafiseh Esmaeil, Chris H L Thio, Ahmad Vaez, Harold Snieder

Abstract read
In one paragraph

Article in Genes, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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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

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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

1 citing paper in PubMed.

  1. 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

5 authors.

Zoha KamaliDepartment of Bioinformatics, Isfahan University of Medical Sciences, Isfahan 81746-73441, Iran.ORCID 0000-0001-6492-5887
Nafiseh EsmaeilDepartment of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan 81746-73441, Iran.
Chris H L ThioDepartment of Epidemiology, University of Groningen, University Medical Centre Groningen, Hanzeplein 1 (9713 GZ), P.O. Box 30.001, 9700 RB Groningen, The Netherlands.ORCID 0000-0003-2623-7172
Ahmad VaezDepartment of Bioinformatics, Isfahan University of Medical Sciences, Isfahan 81746-73441, Iran.ORCID 0000-0001-9048-3795
Harold SniederDepartment of Epidemiology, University of Groningen, University Medical Centre Groningen, Hanzeplein 1 (9713 GZ), P.O. Box 30.001, 9700 RB Groningen, The Netherlands.ORCID 0000-0003-1949-2298

Funding

Isfahan University of Medical Sciences 240257
6 · The paper itself

Abstract

objectivesInterleukin 6 (IL-6) levels at hospital admission have been suggested for disease prognosis, and IL-6 antagonists have been suggested for the treatment of patients with severe COVID-19. However, less is known about the relationship between pre-COVID-19 IL-6 levels and the risk of severe COVID-19. To fill in this gap, here we extensively investigated the association of genetically instrumented IL-6 pathway components with the risk of severe COVID-19.

methodsWe used a two-sample Mendelian randomization study design and retrieved genetic instruments for blood biomarkers of IL-6 activation, including IL-6, soluble IL-6 receptor, IL-6 signal transducer, and CRP, from respective large available GWASs. To establish associations of these instruments with COVID-19 outcomes, we used data from the Host Genetics Initiative and GenOMICC studies.

resultsOur analyses revealed inverse associations of genetically instrumented levels of IL-6 and its soluble receptor with the risk of developing severe disease (OR = 0.60 and 0.94, respectively). They also demonstrated a positive association of severe disease with the soluble signal transducer level (OR = 1.13). Only IL-6 associations with severe COVID-19 outcomes reached the significance threshold corrected for multiple testing (

conclusionsThese potential causal relationships for pre-COVID-19 IL-6 levels with the risk of developing severe symptoms provide opportunities for further evaluation of these factors as prognostic/preventive markers of severe COVID-19. Further studies will need to clarify whether the higher risk for a severe disease course with lower baseline IL-6 levels may also extend to other infectious diseases.

Indexed as

COVID-19Interleukin-6Mendelian Randomization AnalysisReceptors, Interleukin-6SARS-CoV-2BiomarkersGenome-Wide Association StudyHumansPolymorphism, Single NucleotideSignal TransductionBiomarkersIL6 protein, humanIL6R protein, humanInterleukin-6Receptors, Interleukin-6causalityGWASinterleukin 6mendelian randomizationsevere COVID-19

Identifiers

PMID39062668
PMCPMC11275426

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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.