Evidence map›Paper›PMID 33717058›Full record

ArticleFrontiers in immunology2021

Immune Resolution Dilemma: Host Antimicrobial Factor S100A8/A9 Modulates Inflammatory Collateral Tissue Damage During Disseminated Fungal Peritonitis.

Madhu Shankar, Nathalie Uwamahoro, Emelie Backman, Sandra Holmberg, Maria Joanna Niemiec, Johannes Roth, Thomas Vogl, Constantin F Urban

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.9field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 11 citations in OpenAlex.

  1. Review
  2. Article
  3. Neutrophil extracellular traps in homeostasis and disease.Signal transduction and targeted therapy · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
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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

8 authors at 2 institutions in 2 countries.

Madhu ShankarDepartment of Clinical Microbiology, Umeå Centre for Microbial Research (UCMR), Umeå University, Umeå, Sweden.
Nathalie UwamahoroDepartment of Clinical Microbiology, Umeå Centre for Microbial Research (UCMR), Umeå University, Umeå, Sweden.
Emelie BackmanDepartment of Clinical Microbiology, Umeå Centre for Microbial Research (UCMR), Umeå University, Umeå, Sweden.
Sandra HolmbergDepartment of Medical Chemistry and Biophysics, Umeå University, Umeå, Sweden.
Maria Joanna NiemiecDepartment of Clinical Microbiology, Umeå Centre for Microbial Research (UCMR), Umeå University, Umeå, Sweden.
Johannes RothInstitute of Immunology, Universitätsklinikum Münster, University of Münster, Münster, Germany.
Thomas VoglInstitute of Immunology, Universitätsklinikum Münster, University of Münster, Münster, Germany.
Constantin F UrbanDepartment of Clinical Microbiology, Umeå Centre for Microbial Research (UCMR), Umeå University, Umeå, Sweden.
Umeå University · SEUniversity of Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Intra-abdominal infection (peritonitis) is a leading cause of severe disease in surgical intensive care units, as over 70% of patients diagnosed with peritonitis develop septic shock. A critical role of the immune system is to return to homeostasis after combating infection. S100A8/A9 (calprotectin) is an antimicrobial and pro-inflammatory protein complex used as a biomarker for diagnosis of numerous inflammatory disorders. Here we describe the role of S100A8/A9 in inflammatory collateral tissue damage (ICTD). Using a mouse model of disseminated intra-abdominal candidiasis (IAC) in wild-type and S100A8/A9-deficient mice in the presence or absence of S100A9 inhibitor paquinimod, the role of S100A8/A9 during ICTD and fungal clearance were investigated. S100A8/A9-deficient mice developed less ICTD than wild-type mice. Restoration of S100A8/A9 in knockout mice by injection of recombinant protein resulted in increased ICTD and fungal clearance comparable to wild-type levels. Treatment with paquinimod abolished ICTD and S100A9-deficient mice showed increased survival compared to wild-type littermates. The data indicates that S100A8/A9 controls ICTD levels and antimicrobial activity during IAC and that targeting of S100A8/A9 could serve as promising adjunct therapy against this challenging disease.

Indexed as

AnimalsBiomarkersCalgranulin ACalgranulin BColony Count, MicrobialCytokinesDisease Models, AnimalDisease ResistanceDisease SusceptibilityHost-Pathogen InteractionsImmunomodulationInflammation MediatorsMacrophagesMiceMycosesPeritonitisBiomarkersCalgranulin ACalgranulin BCytokinesInflammation MediatorsCandida albicanshost-pathogen interactionshost-targeted agentsinflammationperitonitisS100A8/A9 complexsepsis

Identifiers

PMID33717058
PMCPMC7953150
OpenAlexW3134320655

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.