Student or educator? Sign up with your school email and get 6 months of Pro free.
CoChat
Sign Up
Cited by 356

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Myeloid-derived miR-223 regulates intestinal inflammation via repression of the NLRP3 inflammasome

Neudecker, Viola, Haneklaus, Moritz, Jensen, Owen, Khailova, Ludmila, Masterson, Joanne C., Tye, Hazel, Biette, Kathryn, Jedlicka, Paul, Brodsky, Kelley S., Gerich, Mark E., Mack, Matthias, Robertson, Avril A.B., Cooper, Matthew A., Furuta, Glenn T., Dinarello, Charles A., O’Neill, Luke A., Eltzschig, Holger K., Masters, Seth L., McNamee, Eóin N.·2017·Journal of Experimental Medicine
DOI 10.1084/jem.20160462
Open this paper in CoChat — free account

Abstract

MicroRNA (miRNA)-mediated RNA interference regulates many immune processes, but how miRNA circuits orchestrate aberrant intestinal inflammation during inflammatory bowel disease (IBD) is poorly defined. Here, we report that miR-223 limits intestinal inflammation by constraining the nlrp3 inflammasome. miR-223 was increased in intestinal biopsies from patients with active IBD and in preclinical models of intestinal inflammation. miR-223-/y mice presented with exacerbated myeloid-driven experimental colitis with heightened clinical, histopathological, and cytokine readouts. Mechanistically, enhanced NLRP3 inflammasome expression with elevated IL-1β was a predominant feature during the initiation of colitis with miR-223 deficiency. Depletion of CCR2+ inflammatory monocytes and pharmacologic blockade of IL-1β or NLRP3 abrogated this phenotype. Generation of a novel mouse line, with deletion of the miR-223 binding site in the NLRP3 3′ untranslated region, phenocopied the characteristics of miR-223-/y mice. Finally, nanoparticle-mediated overexpression of miR-223 attenuated experimental colitis, NLRP3 levels, and IL-1β release. Collectively, our data reveal a previously unappreciated role for miR-223 in regulating the innate immune response during intestinal inflammation.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1084/jem.20160462

Cites

6 of 6 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 6 references

Research works printed but not linked: 43

  1. Andres, 2000, Mice with a selective deletion of the CC chemokine receptors 5 or 2 are protected from dextran sodium sulfate-mediated colitis: Lack of CC chemokine receptor 5 expression results in a NK1.1+ lymphocyte-associated Th2-type immune response in the intestine, J. Immunol., 164, 6303, 10.4049/jimmunol.164.12.6303 · DOI · Paper page
  2. Bamias, 2012, New insights into the dichotomous role of innate cytokines in gut homeostasis and inflammation, Cytokine., 59, 451, 10.1016/j.cyto.2012.06.014 · DOI
  3. Bauer, 2010, Colitis induced in mice with dextran sulfate sodium (DSS) is mediated by the NLRP3 inflammasome, Gut., 59, 1192, 10.1136/gut.2009.197822 · DOI · Paper page
  4. Bauernfeind, 2012, NLRP3 inflammasome activity is negatively controlled by miR-223, J. Immunol., 189, 4175, 10.4049/jimmunol.1201516 · DOI · Paper page
  5. Bersudsky, 2014, Non-redundant properties of IL-1α and IL-1β during acute colon inflammation in mice, Gut., 63, 598, 10.1136/gutjnl-2012-303329 · DOI · Paper page
  6. Brazil, 2013, The role of polymorphonuclear leukocyte trafficking in the perpetuation of inflammation during inflammatory bowel disease, Inflamm. Bowel Dis., 19, 1556, 10.1097/MIB.0b013e318281f54e · DOI
  7. Calkins, 2002, IL-1 regulates in vivo C-X-C chemokine induction and neutrophil sequestration following endotoxemia, J. Endotoxin Res., 8, 59
  8. Casini-Raggi, 1995, Mucosal imbalance of IL-1 and IL-1 receptor antagonist in inflammatory bowel disease. A novel mechanism of chronic intestinal inflammation, J. Immunol., 154, 2434, 10.4049/jimmunol.154.5.2434 · DOI · Paper page
  9. Cominelli, 1990, Interleukin 1 suppresses inflammation in rabbit colitis. Mediation by endogenous prostaglandins, J. Clin. Invest., 85, 582, 10.1172/JCI114476 · DOI
  10. Dorhoi, 2013, MicroRNA-223 controls susceptibility to tuberculosis by regulating lung neutrophil recruitment, J. Clin. Invest., 123, 4836, 10.1172/JCI67604 · DOI · Paper page
  11. Elinav, 2011, NLRP6 inflammasome regulates colonic microbial ecology and risk for colitis, Cell., 145, 745, 10.1016/j.cell.2011.04.022 · DOI · Paper page
  12. Eulalio, 2012, The mammalian microRNA response to bacterial infections, RNA Biol., 9, 742, 10.4161/rna.20018 · DOI · Paper page
  13. Gentner, 2009, Stable knockdown of microRNA in vivo by lentiviral vectors, Nat. Methods., 6, 63, 10.1038/nmeth.1277 · DOI · Paper page
  14. Haneklaus, 2012, Cutting edge: miR-223 and EBV miR-BART15 regulate the NLRP3 inflammasome and IL-1β production, J. Immunol., 189, 3795, 10.4049/jimmunol.1200312 · DOI · Paper page
  15. Haneklaus, 2013, miR-223: Infection, inflammation and cancer, J. Intern. Med., 274, 215, 10.1111/joim.12099 · DOI · Paper page
  16. Hsu, 2012, Essential metabolic, anti-inflammatory, and anti-tumorigenic functions of miR-122 in liver, J. Clin. Invest., 122, 2871, 10.1172/JCI63539 · DOI · Paper page
  17. Huang, 2006, RegRNA: An integrated web server for identifying regulatory RNA motifs and elements, Nucleic Acids Res., 34, W429, 10.1093/nar/gkl333 · DOI · Paper page
  18. Janssen, 2013, Treatment of HCV infection by targeting microRNA, N. Engl. J. Med., 368, 1685, 10.1056/NEJMoa1209026 · DOI · Paper page
  19. Johnnidis, 2008, Regulation of progenitor cell proliferation and granulocyte function by microRNA-223, Nature., 451, 1125, 10.1038/nature06607 · DOI · Paper page
  20. Karmakar, 2015, Neutrophil IL-1β processing induced by pneumolysin is mediated by the NLRP3/ASC inflammasome and caspase-1 activation and is dependent on K+ efflux, J. Immunol., 194, 1763, 10.4049/jimmunol.1401624 · DOI · Paper page
  21. Li, 2010, MicroRNAs modulate the noncanonical transcription factor NF-κB pathway by regulating expression of the kinase IKKα during macrophage differentiation, Nat. Immunol., 11, 799, 10.1038/ni.1918 · DOI · Paper page
  22. Ligumsky, 1990, Role of interleukin 1 in inflammatory bowel disease: Enhanced production during active disease, Gut., 31, 686, 10.1136/gut.31.6.686 · DOI · Paper page
  23. Lopetuso, 2013, Opposing functions of classic and novel IL-1 family members in gut health and disease, Front. Immunol., 4, 181, 10.3389/fimmu.2013.00181 · DOI
  24. Mankan, 2012, The NLRP3/ASC/caspase-1 axis regulates IL-1β processing in neutrophils, Eur. J. Immunol., 42, 710, 10.1002/eji.201141921 · DOI · Paper page
  25. McNamee, 2010, Novel model of TH2-polarized chronic ileitis: the SAMP1 mouse, Inflamm. Bowel Dis., 16, 743, 10.1002/ibd.21148 · DOI
  26. McNamee, 2011, Interleukin 37 expression protects mice from colitis, Proc. Natl. Acad. Sci. USA., 108, 16711, 10.1073/pnas.1111982108 · DOI · Paper page
  27. Mosser, 2008, Activation of murine macrophages, Curr. Protoc. Immunol., Chapter 14, Unit 14.2, 10.1002/0471142735.im1402s83 · DOI · Paper page
  28. Nagler-Anderson, 2001, Man the barrier! Strategic defences in the intestinal mucosa, Nat. Rev. Immunol., 1, 59, 10.1038/35095573 · DOI · Paper page
  29. Nowarski, 2015, Epithelial IL-18 equilibrium controls barrier function in colitis, Cell., 163, 1444, 10.1016/j.cell.2015.10.072 · DOI · Paper page
  30. O’Connell, 2010, Physiological and pathological roles for microRNAs in the immune system, Nat. Rev. Immunol., 10, 111, 10.1038/nri2708 · DOI · Paper page
  31. Polytarchou, 2015, Assessment of circulating microRNAs for the diagnosis and disease activity evaluation in patients with ulcerative colitis by using the nanostring technology, Inflamm. Bowel Dis., 21, 2533, 10.1097/MIB.0000000000000547 · DOI
  32. Pulikkan, 2010, Cell-cycle regulator E2F1 and microRNA-223 comprise an autoregulatory negative feedback loop in acute myeloid leukemia, Blood., 115, 1768, 10.1182/blood-2009-08-240101 · DOI · Paper page
  33. Ramkissoon, 2006, Hematopoietic-specific microRNA expression in human cells, Leuk. Res., 30, 643, 10.1016/j.leukres.2005.09.001 · DOI · Paper page
  34. Reinecker, 1993, Enhanced secretion of tumour necrosis factor-alpha, IL-6, and IL-1β by isolated lamina propria mononuclear cells from patients with ulcerative colitis and Crohn’s disease, Clin. Exp. Immunol., 94, 174, 10.1111/j.1365-2249.1993.tb05997.x · DOI · Paper page
  35. Satsangi, 2006, The Montreal classification of inflammatory bowel disease: Controversies, consensus, and implications, Gut., 55, 749, 10.1136/gut.2005.082909 · DOI · Paper page
  36. Schaefer, 2011, Selective upregulation of microRNA expression in peripheral blood leukocytes in IL-10-/- mice precedes expression in the colon, J. Immunol., 187, 5834, 10.4049/jimmunol.1100922 · DOI
  37. Seo, 2015, Distinct commensals induce interleukin-1β via NLRP3 inflammasome in inflammatory monocytes to promote intestinal inflammation in response to injury, Immunity., 42, 744, 10.1016/j.immuni.2015.03.004 · DOI · Paper page
  38. Shouval, 2016, Interleukin 1β mediates intestinal inflammation in mice and patients with interleukin 10 receptor deficiency, Gastroenterology., 151, 1100, 10.1053/j.gastro.2016.08.055 · DOI · Paper page
  39. Song-Zhao, 2014, Nlrp3 activation in the intestinal epithelium protects against a mucosal pathogen, Mucosal Immunol., 7, 763, 10.1038/mi.2013.94 · DOI
  40. Zaki, 2010, The NLRP3 inflammasome protects against loss of epithelial integrity and mortality during experimental colitis, Immunity., 32, 379, 10.1016/j.immuni.2010.03.003 · DOI · Paper page
  41. Zhang, 2014, Inflammasome activation has an important role in the development of spontaneous colitis, Mucosal Immunol., 7, 1139, 10.1038/mi.2014.1 · DOI
  42. Zhou, 2015, MicroRNA-223 regulates the differentiation and function of intestinal dendritic cells and macrophages by targeting C/EBPβ, Cell Reports., 13, 1149, 10.1016/j.celrep.2015.09.073 · DOI · Paper page
  43. Zigmond, 2012, Ly6C hi monocytes in the inflamed colon give rise to proinflammatory effector cells and migratory antigen-presenting cells, Immunity., 37, 1076, 10.1016/j.immuni.2012.08.026 · DOI · Paper page

Cited by

See all 356

Metadata

Authors
Neudecker, V., Haneklaus, M., Jensen, O., Khailova, L., Masterson, J. C., Tye, H., Biette, K., Jedlicka, P., Brodsky, K. S., Gerich, M. E., Mack, M., Robertson, A. A. B., Cooper, M. A., Furuta, G. T., Dinarello, C. A., O’Neill, L. A., Eltzschig, H. K., Masters, S. L., & McNamee, E. N.
Affiliations
  • Clinic for Anesthesiology, University Hospital of Ludwig-Maximilians-University, 80539 Munich, Germany 1
  • School of Biochemistry and Immunology, Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin 2, Ireland 2
  • Mucosal Inflammation Program, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045 13
  • Department of Anesthesiology, School of Medicine, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045 14
  • Gastrointestinal Eosinophilic Disease Program, Section of Pediatric Gastroenterology, Hepatology, and Nutrition, Children's Hospital Colorado, Aurora, CO 80045 3
  • Division of Inflammation, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC 3052, Australia 4
  • Department of Pathology, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045 10
  • Division of Gastroenterology and Hepatology, University of Colorado, Anschutz Medical Campus, Aurora, CO 80045 11
  • Department of Internal Medicine II, University Hospital Regensburg, 93053 Regensburg, Germany 6
  • Institute for Molecular Bioscience, The University of Queensland, Brisbane City, QLD 4067, Australia 7
  • Department of Medicine, Radboud University Medical Center, 6525 GA Nijmegen, Netherlands 9
  • Department of Anesthesiology, University of Texas Medical School at Houston, Houston, TX 77030 8
ORCID
Venue
Journal of Experimental Medicine
Publisher
Rockefeller University Press
Published
2017-05-09
Volume
214
Issue
6
Pages
1737-1752
ISSN
  • 0022-1007
  • 1540-9538
DOI
10.1084/jem.20160462
Cited by
356
References
6
Language
en
Licence
Funders
  • German Research Foundation
  • American Heart Association
  • National Institutes of Health (K01DK106315, R01 DK097075, R01- HL098294, POI-HL114457, R01-DK082509, R01-HL109233, R01-DK109574, R01-HL119837, R01-HL133900)
  • NASPGHAN Foundation
  • Crohn’s and Colitis Foundation of America (3760)
  • National Health and Medical Research Council (1057815, 1099262, 361646)
  • Victorian Endowment for Science Knowledge and Innovation
  • State Government of Victoria
  • GlaxoSmithKline
  • CCFA (273007, 409992)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

How to cite

Cite CoChat for the checks on this page, and the paper for its own findings.

This page
CoChat. (2026). Citation check: Myeloid-derived miR-223 regulates intestinal inflammation via repression of the NLRP3 inflammasome. https://app.cochat.ai/papers/10.1084/jem.20160462
The paper
Neudecker, V., Haneklaus, M., Jensen, O., Khailova, L., Masterson, J. C., Tye, H., Biette, K., Jedlicka, P., Brodsky, K. S., Gerich, M. E., Mack, M., Robertson, A. A. B., Cooper, M. A., Furuta, G. T., Dinarello, C. A., O’Neill, L. A., Eltzschig, H. K., Masters, S. L., & McNamee, E. N. (2017). Myeloid-derived miR-223 regulates intestinal inflammation via repression of the NLRP3 inflammasome. Journal of Experimental Medicine. https://doi.org/10.1084/jem.20160462

Data sources

Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.