Evidence map›Paper›PMID 26555704›Full record

ArticleMucosal immunology2016

MMP-19 deficiency causes aggravation of colitis due to defects in innate immune cell function.

R Brauer, J Tureckova, I Kanchev, M Khoylou, J Skarda, J Prochazka, F Spoutil, I M Beck, O Zbodakova, P Kasparek and 7 more

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
0.7field-weighted citation impact, top 21% 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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Diabetes and Immunosuppression Drive Distinct Patterns ofbioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. The NEDD8-activating enzyme inhibitor MLN4924 reduces ischemic brain injury in mice.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  12. Review
  13. Article
  14. Digestive Inflammation: Role of Proteolytic Dysregulation.International journal of molecular sciences · 2021
    Review
  15. Review
  16. Article
  17. Review
  18. 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

17 authors at 5 institutions in 3 countries.

R BrauerInstitute of Molecular Genetics of the ASCR, Laboratory of Transgenic Models of Diseases, Prague, Czech Republic.
J TureckovaInstitute of Molecular Genetics of the ASCR, Laboratory of Transgenic Models of Diseases, Prague, Czech Republic.
I KanchevInstitute of Molecular Genetics of the ASCR, Laboratory of Transgenic Models of Diseases, Prague, Czech Republic.
M KhoylouInstitute of Molecular and Translational Medicine, Faculty of Medicine and Dentistry, Palacky University and University Hospital in Olomouc, Olomouc, Czech Republic.
J SkardaDepartment of Clinical and Molecular Pathology, Faculty of Medicine and Dentistry, Palacky University and University Hospital in Olomouc, Olomouc, Czech Republic.
J ProchazkaInstitute of Molecular Genetics of the ASCR, Laboratory of Transgenic Models of Diseases, Prague, Czech Republic.
F SpoutilInstitute of Molecular Genetics of the ASCR, Laboratory of Transgenic Models of Diseases, Prague, Czech Republic.
I M BeckInstitute of Molecular Genetics of the ASCR, Laboratory of Transgenic Models of Diseases, Prague, Czech Republic.
O ZbodakovaInstitute of Molecular Genetics of the ASCR, Laboratory of Transgenic Models of Diseases, Prague, Czech Republic.
P KasparekInstitute of Molecular Genetics of the ASCR, Laboratory of Transgenic Models of Diseases, Prague, Czech Republic.
V KorinekInstitute of Molecular Genetics of the ASCR, Laboratory of Transgenic Models of Diseases, Prague, Czech Republic.
K ChalupskyInstitute of Molecular Genetics of the ASCR, Laboratory of Transgenic Models of Diseases, Prague, Czech Republic.
T KarhuInstitute of Biomedicine and Biocenter of Oulu, Medical Research Center Oulu, Oulu University Hospital, Oulu, Finland.
K-H HerzigInstitute of Biomedicine and Biocenter of Oulu, Medical Research Center Oulu, Oulu University Hospital, Oulu, Finland.
M HajduchInstitute of Molecular and Translational Medicine, Faculty of Medicine and Dentistry, Palacky University and University Hospital in Olomouc, Olomouc, Czech Republic.
M GregorInstitute of Molecular Genetics of the ASCR, Laboratory of Transgenic Models of Diseases, Prague, Czech Republic.
R SedlacekInstitute of Molecular Genetics of the ASCR, Laboratory of Transgenic Models of Diseases, Prague, Czech Republic.
Czech Academy of Sciences, Institute of Molecular Genetics · CZOulu University Hospital · FIPalacký University Olomouc · CZInstitute of Molecular and Translational Medicine · CZLung Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Matrix metalloproteinases (MMPs) are potential biomarkers for disease activity in inflammatory bowel disease (IBD). However, clinical trials targeting MMPs have not succeeded, likely due to poor understanding of the biological functions of individual MMPs. Here, we explore the role of MMP-19 in IBD pathology. Using a DSS-induced model of colitis, we show evidence for increased susceptibility of Mmp-19-deficient (Mmp-19(-/-)) mice to colitis. Absence of MMP-19 leads to significant disease progression, with reduced survival rates, severe tissue destruction, and elevated levels of pro-inflammatory modulators in the colon and plasma, and failure to resolve inflammation. There was a striking delay in neutrophil infiltration into the colon of Mmp-19(-/-) mice during the acute colitis, leading to persistent inflammation and poor recovery; this was rescued by reconstitution of irradiated Mmp-19(-/-) mice with wild-type bone marrow. Additionally, Mmp-19-deficient macrophages exhibited decreased migration in vivo and in vitro and the mucosal barrier appeared compromised. Finally, chemokine fractalkine (CX3CL1) was identified as a novel substrate of MMP-19, suggesting a link between insufficient processing of CX3CL1 and cell recruitment in the Mmp-19(-/-) mice. MMP-19 proves to be a critical factor in balanced host response to colonic pathogens, and for orchestrating appropriate innate immune response in colitis.

Indexed as

AnimalsCell MovementCells, CulturedChemokine CX3CL1ColitisColonCytokinesDextran SulfateDisease ProgressionHumansImmunity, InnateInflammation MediatorsInflammatory Bowel DiseasesIntestinal MucosaMacrophagesMatrix Metalloproteinases, SecretedChemokine CX3CL1Cx3cl1 protein, mouseCytokinesDextran SulfateInflammation Mediatorsmatrix metalloproteinase 19Matrix Metalloproteinases, Secreted

Identifiers

PMID26555704
OpenAlexW2338623938

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.