Evidence map›Paper›PMID 24084739›Full record

ArticleThe Journal of clinical investigation2013

MicroRNA-223 controls susceptibility to tuberculosis by regulating lung neutrophil recruitment.

Anca Dorhoi, Marco Iannaccone, Maura Farinacci, Kellen C Faé, Jörg Schreiber, Pedro Moura-Alves, Geraldine Nouailles, Hans-Joachim Mollenkopf, Dagmar Oberbeck-Müller, Sabine Jörg and 7 more

Registry-linked trialAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04815811 (Study of the Sex Differences in Inflammatory Diseases in Children), which is not on this map. Cited by 175 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
175citing papers in PubMed, 2 pooled it
8.5field-weighted citation impact, top 2% 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.

NCT04815811 naunknown statusnot on this mapstarted 2019, after this paper: background citation

Study of the Sex Differences in Inflammatory Diseases in Children

TypeinterventionalSponsorQueen Fabiola Children's University HospitalRan2019 to 2023Enrolled160ConditionsSex Differences in Immune Response, Acute Inflammatory Diseases in ChildrenArmsBlood collection, Stool collection
3 · Its place in the literature

Who cites it

175 citing papers in PubMed, 2 syntheses or guidelines pooled it, 288 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Extracellular vesicle-mediated mechanisms and therapeutic potential in acute lung injury.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Skeletal Muscle as Endocrine Organ.Advances in experimental medicine and biology · 2025
    Review
  14. Article
  15. Epigenetic Mechanisms Induced byInternational journal of molecular sciences · 2024
    Review
  16. Article
  17. Article
  18. Review
  19. Lung Inflammation Signature in Post-COVID-19 TB Patients.International journal of molecular sciences · 2023
    Article
  20. Review

115 more citing papers are in PubMed but not listed here.

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

17 authors at 4 institutions in 2 countries.

Anca Dorhoi
Marco Iannaccone
Maura Farinacci
Kellen C Faé
Jörg Schreiber
Pedro Moura-Alves
Geraldine Nouailles
Hans-Joachim Mollenkopf
Dagmar Oberbeck-Müller
Sabine Jörg
Ellen Heinemann
Karin Hahnke
Delia Löwe
Franca Del Nonno
Delia Goletti
Rosanna Capparelli
Stefan H E Kaufmann
Max Planck Institute for Infection Biology · DEMax Planck Society · DEIstituto Nazionale per le Malattie Infettive Lazzaro Spallanzani · ITUniversity of Naples Federico II · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The molecular mechanisms that control innate immune cell trafficking during chronic infection and inflammation, such as in tuberculosis (TB), are incompletely understood. During active TB, myeloid cells infiltrate the lung and sustain local inflammation. While the chemoattractants that orchestrate these processes are increasingly recognized, the posttranscriptional events that dictate their availability are unclear. We identified microRNA-223 (miR-223) as an upregulated small noncoding RNA in blood and lung parenchyma of TB patients and during murine TB. Deletion of miR-223 rendered TB-resistant mice highly susceptible to acute lung infection. The lethality of miR-223(–/–) mice was apparently not due to defects in antimycobacterial T cell responses. Exacerbated TB in miR-223(–/–) animals could be partially reversed by neutralization of CXCL2, CCL3, and IL-6, by mAb depletion of neutrophils, and by genetic deletion of Cxcr2. We found that miR-223 controlled lung recruitment of myeloid cells, and consequently, neutrophil-driven lethal inflammation. We conclude that miR-223 directly targets the chemoattractants CXCL2, CCL3, and IL-6 in myeloid cells. Our study not only reveals an essential role for a single miRNA in TB, it also identifies new targets for, and assigns biological functions to, miR-223. By regulating leukocyte chemotaxis via chemoattractants, miR-223 is critical for the control of TB and potentially other chronic inflammatory diseases.

Indexed as

AnimalsChemokine CCL3Chemokine CXCL2Disease SusceptibilityHumansImmunity, InnateInterleukin-6LungMiceMice, Inbred C57BLMice, KnockoutMicroRNAsNeutrophil InfiltrationReceptors, Interleukin-8BTuberculosis, PulmonaryUp-RegulationCcl3 protein, mouseChemokine CCL3Chemokine CXCL2Cxcl2 protein, mouseInterleukin-6MicroRNAsMIR223, humanMIRN223 microRNA, mouseReceptors, Interleukin-8B

Identifiers

PMID24084739
PMCPMC3809781
OpenAlexW2080595107

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.