Evidence map›Paper›PMID 38768576›Full record

ArticleJournal of innate immunity2024

The Inflammatory Response Induced by Aspergillus fumigatus Conidia Is Dependent on Complement Activation: Insight from a Whole Blood Model.

Beatrice Fageräng, Maximilian Peter Götz, Leon Cyranka, Corinna Lau, Per H Nilsson, Tom Eirik Mollnes, Peter Garred

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PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of innate immunity, 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

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

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

7 authors.

Beatrice FagerängDepartment of Immunology, Oslo University Hospital, University of Oslo, Oslo, Norway.
Maximilian Peter GötzLaboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, Rigshospitalet, and Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Leon CyrankaLaboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, Rigshospitalet, and Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Corinna LauResearch Laboratory, Nordland Hospital, Bodø, Norway.
Per H NilssonDepartment of Immunology, Oslo University Hospital, University of Oslo, Oslo, Norway.
Tom Eirik MollnesDepartment of Immunology, Oslo University Hospital, University of Oslo, Oslo, Norway.
Peter GarredLaboratory of Molecular Medicine, Department of Clinical Immunology, Section 7631, Rigshospitalet, and Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionWe aimed to elucidate the inflammatory response of Aspergillus fumigatus conidia in a whole-blood model of innate immune activation and to compare it with the well-characterized inflammatory reaction to Escherichia coli.

methodsEmploying a human lepirudin whole-blood model, we analyzed complement and leukocyte activation by measuring the sC5b-9 complex and assessing CD11b expression. A 27-multiplex system was used for quantification of cytokines. Selective cell removal from whole blood and inhibition of C3, C5, and CD14 were also applied.

resultsOur findings demonstrated a marked elevation in sC5b-9 and CD11b post-A. fumigatus incubation. Thirteen cytokines (TNF, IL-1β, IL-1ra, IL-4, IL-6, IL-8, IL-17, IFNγ, MCP-1, MIP-1α, MIP-1β, FGF-basic, and G-CSF) showed increased levels. A generally lower level of cytokine release and CD11b expression was observed with A. fumigatus conidia than with E. coli. Notably, monocytes were instrumental in releasing all cytokines except MCP-1. IL-1ra was found to be both monocyte and granulocyte-dependent. Pre-inhibiting with C3 and CD14 inhibitors resulted in decreased release patterns for six cytokines (TNF, IL-1β, IL-6, IL-8, MIP-1α, and MIP-1β), with minimal effects by C5-inhibition.

conclusionA. fumigatus conidia induced complement activation comparable to E. coli, whereas CD11b expression and cytokine release were lower, underscoring distinct inflammatory responses between these pathogens. Complement C3 inhibition attenuated cytokine release indicating a C3-level role of complement in A. fumigatus immunity.

Indexed as

AspergillosisAspergillus fumigatusComplement ActivationCytokinesEscherichia coliSpores, FungalCD11b AntigenCells, CulturedComplement C3Complement Membrane Attack ComplexHumansImmunity, InnateInflammationLipopolysaccharide ReceptorsMonocytesCD11b AntigenComplement C3Complement Membrane Attack ComplexCytokinesLipopolysaccharide ReceptorsAspergillus fumigatusCD14ComplementCytokinesInflammatory responseToll-like receptors

Identifiers

PMID38768576
PMCPMC11250388

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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.