Evidence map›Paper›PMID 26293821›Full record

ArticleJournal of the American Society of Nephrology : JASN2016

Hepcidin as a Major Component of Renal Antibacterial Defenses against Uropathogenic Escherichia coli.

Dounia Houamel, Nicolas Ducrot, Thibaud Lefebvre, Raed Daher, Boualem Moulouel, Marie-Agnes Sari, Philippe Letteron, Said Lyoumi, Sarah Millot, Jerome Tourret and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
4.4field-weighted citation impact, top 5% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

  1. Pooled it
  2. Hepcidin and Tissue-Specific Iron Regulatory Networks.Advances in experimental medicine and biology · 2025
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Uropathogen and host responses in pyelonephritis.Nature reviews. Nephrology · 2023
    Review
  11. Article
  12. Repurposing HDAC inhibitors to enhance ribonuclease 4 and 7 expression and reduce urinary tract infection.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  13. Article
  14. Article
  15. Expression and function of human ribonuclease 4 in the kidney and urinary tract.American journal of physiology. Renal physiology · 2021
    Article
  16. Iron Therapeutics in Women's Health: Past, Present, and Future.Pharmaceuticals (Basel, Switzerland) · 2020
    Review
  17. Article
  18. Review
  19. Innate immunity and urinary tract infection.Pediatric nephrology (Berlin, Germany) · 2020
    Review
  20. 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

18 authors at 8 institutions in 1 country.

Dounia HouamelNational Institute of Health and Medical Research (INSERM) U1149, Research Centre on inflammation, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; Laboratory of Excellence, GR-Ex, Paris, France;
Nicolas DucrotNational Institute of Health and Medical Research (INSERM) U1149, Research Centre on inflammation, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; Laboratory of Excellence, GR-Ex, Paris, France;
Thibaud LefebvreNational Institute of Health and Medical Research (INSERM) U1149, Research Centre on inflammation, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; Laboratory of Excellence, GR-Ex, Paris, France; AP-HP, French Center for Porphyrias, Louis Mourier Hospital, Colombes, France;
Raed DaherNational Institute of Health and Medical Research (INSERM) U1149, Research Centre on inflammation, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; Laboratory of Excellence, GR-Ex, Paris, France;
Boualem MoulouelNational Institute of Health and Medical Research (INSERM) U1149, Research Centre on inflammation, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; Laboratory of Excellence, GR-Ex, Paris, France;
Marie-Agnes SariThe National Centre for Scientific Research (CNRS), UMR 8601, Descartes University, Paris, France;
Philippe LetteronNational Institute of Health and Medical Research (INSERM) U1149, Research Centre on inflammation, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France;
Said LyoumiNational Institute of Health and Medical Research (INSERM) U1149, Research Centre on inflammation, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; Laboratory of Excellence, GR-Ex, Paris, France;
Sarah MillotNational Institute of Health and Medical Research (INSERM) U1149, Research Centre on inflammation, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; Laboratory of Excellence, GR-Ex, Paris, France;
Jerome TourretParis Diderot University, Sorbonne Paris Cité, Paris, France; INSERM U1137, Infection Antimicrobials Modelling Evolution (IAME) Laboratory, Paris, France; and.
Odile BouvetParis Diderot University, Sorbonne Paris Cité, Paris, France; INSERM U1137, Infection Antimicrobials Modelling Evolution (IAME) Laboratory, Paris, France; and.
Sophie VaulontLaboratory of Excellence, GR-Ex, Paris, France; INSERM U1016, Cochin Institute, Descartes University, Paris, France.
Alain VandewalleNational Institute of Health and Medical Research (INSERM) U1149, Research Centre on inflammation, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France;
Erick DenamurParis Diderot University, Sorbonne Paris Cité, Paris, France; INSERM U1137, Infection Antimicrobials Modelling Evolution (IAME) Laboratory, Paris, France; and.
Hervé PuyNational Institute of Health and Medical Research (INSERM) U1149, Research Centre on inflammation, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; Laboratory of Excellence, GR-Ex, Paris, France; AP-HP, French Center for Porphyrias, Louis Mourier Hospital, Colombes, France;
Carole BeaumontNational Institute of Health and Medical Research (INSERM) U1149, Research Centre on inflammation, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; Laboratory of Excellence, GR-Ex, Paris, France;
Laurent GouyaNational Institute of Health and Medical Research (INSERM) U1149, Research Centre on inflammation, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; Laboratory of Excellence, GR-Ex, Paris, France; AP-HP, French Center for Porphyrias, Louis Mourier Hospital, Colombes, France;
Zoubida KarimNational Institute of Health and Medical Research (INSERM) U1149, Research Centre on inflammation, Paris, France; Paris Diderot University, Sorbonne Paris Cité, Paris, France; Laboratory of Excellence, GR-Ex, Paris, France; zoubida.karim@inserm.fr.
Centre de Recherche sur l'Inflammation · FRUniversité Paris Cité · FRSorbonne Paris Cité · FRDélégation Paris 7 · FRLaboratory of Excellence GR-Ex · FRAssistance Publique – Hôpitaux de Paris · FRCentre National de la Recherche Scientifique · FRInstitut Cochin · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The iron-regulatory peptide hepcidin exhibits antimicrobial activity. Having previously shown hepcidin expression in the kidney, we addressed its role in urinary tract infection (UTI), which remains largely unknown. Experimental UTI was induced in wild-type (WT) and hepcidin-knockout (Hepc-/-) mice using the uropathogenic Escherichia coli CFT073 strain. Compared with infected WT mice, infected Hepc-/- mice showed a dramatic increase in renal bacterial load. Moreover, bacterial invasion was significantly dampened by the pretreatment of WT mice with hepcidin. Infected Hepc-/- mice exhibited decreased iron accumulation in the renal medulla and significant attenuation of the renal inflammatory response. Notably, we demonstrated in vitro bacteriostatic activity of hepcidin against CFT073. Furthermore, CFT073 repressed renal hepcidin, both in vivo and in cultured renal cells, and reduced phosphorylation of SMAD kinase in vivo, suggesting a bacterial strategy to escape the antimicrobial activities of hepcidin. In conclusion, we provide new mechanisms by which hepcidin contributes to renal host defense and suggest that targeting hepcidin offers a strategy to prevent bacterial invasion.

Indexed as

AnimalsAnti-Infective AgentsBacterial LoadCells, CulturedColony Count, MicrobialCytokinesEscherichia coliEscherichia coli InfectionsFemaleHepcidinsIronKidney MedullaMiceMice, Inbred CBAMice, KnockoutNephritisAnti-Infective AgentsCytokinesHepcidinsIronRNA, MessengerSmad ProteinsStat3 protein, mouseSTAT3 Transcription Factorcell and transport physiologycell signalingkidney diseasepyelonephritisrenal epithelial cellrenal protection

Identifiers

PMID26293821
PMCPMC4769187
OpenAlexW1945885800

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.