Evidence map›Paper›PMID 40182015›Full record

ArticleHemaSphere2025

Hepatocyte Toll-like receptors contribute to the hepcidin inflammatory response to pathogens and pathogen-derived ligands.

Katharina Bonitz, Silvia Colucci, Ruiyue Qiu, Sandro Altamura, Richard Sparla, Katja Mudder, Stefan Zimmermann, Matthias W Hentze, Martina U Muckenthaler, Oriana Marques

Abstract read
In one paragraph

Article in HemaSphere, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. mBio · 2026
    Article
  5. Review
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  7. 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

10 authors.

Katharina BonitzDepartment of Pediatric Oncology, Hematology and Immunology Hopp Children's Cancer Center (KiTZ), University Hospital Heidelberg Heidelberg Germany.
Silvia ColucciDepartment of Pediatric Oncology, Hematology and Immunology Hopp Children's Cancer Center (KiTZ), University Hospital Heidelberg Heidelberg Germany.ORCID https://orcid.org/0000-0002-0816-9009
Ruiyue QiuDepartment of Pediatric Oncology, Hematology and Immunology Hopp Children's Cancer Center (KiTZ), University Hospital Heidelberg Heidelberg Germany.
Sandro AltamuraDepartment of Pediatric Oncology, Hematology and Immunology Hopp Children's Cancer Center (KiTZ), University Hospital Heidelberg Heidelberg Germany.ORCID https://orcid.org/0000-0002-6781-1073
Richard SparlaDepartment of Pediatric Oncology, Hematology and Immunology Hopp Children's Cancer Center (KiTZ), University Hospital Heidelberg Heidelberg Germany.
Katja MudderDepartment of Pediatric Oncology, Hematology and Immunology Hopp Children's Cancer Center (KiTZ), University Hospital Heidelberg Heidelberg Germany.
Stefan ZimmermannDepartment of Infectious Diseases, Microbiology and Hygiene University Hospital Heidelberg Heidelberg Germany.
Matthias W HentzeMolecular Medicine Partnership Unit (MMPU) EMBL University of Heidelberg Heidelberg Germany.
Martina U MuckenthalerDepartment of Pediatric Oncology, Hematology and Immunology Hopp Children's Cancer Center (KiTZ), University Hospital Heidelberg Heidelberg Germany.ORCID 0000-0002-3778-510X
Oriana MarquesDepartment of Pediatric Oncology, Hematology and Immunology Hopp Children's Cancer Center (KiTZ), University Hospital Heidelberg Heidelberg Germany.ORCID https://orcid.org/0000-0003-4670-2748

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Iron restriction is a critical pathomechanism underlying the Anemia of Inflammation and an innate immune response limiting the replication of extracellular pathogens. During infections, innate immune cells detect pathogen-associated molecular patterns (PAMPs) and produce proinflammatory cytokines. Among these, interleukin (IL)-6 is detected by hepatocytes, where it activates the production of the iron-regulated hormone hepcidin that inhibits iron export from macrophages. Consequently, macrophages accumulate iron and hypoferremia (low plasma iron) develops. Whether Toll-like receptors (TLRs) expressed on hepatocytes directly recognize PAMPs and contribute to hepcidin upregulation is still an open question. Stimulation of primary murine hepatocytes with a panel of PAMPs targeting TLRs 1-9 revealed that the TLR5 ligand flagellin and the TLR2:TLR6 ligand FSL1 upregulated hepcidin. Hepcidin was also induced upon treatment with heat-killed

Identifiers

PMID40182015
PMCPMC11966559

What OpenQuestion holds

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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.