Evidence map›Paper›PMID 18627421›Full record

ArticleJournal of cellular and molecular medicine2009

Osteopontin as two-sided mediator of intestinal inflammation.

Katja Heilmann, Ute Hoffmann, Ellen Witte, Christoph Loddenkemper, Christian Sina, Stefan Schreiber, Claudia Hayford, Pamela Holzlöhner, Kerstin Wolk, Elianne Tchatchou and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.1field-weighted citation impact, top 7% 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

48 citing papers in PubMed, 77 citations in OpenAlex.

  1. Article
  2. The functional role of the extracellular matrix in inflammatory bowel disease associated gut fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2025
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  10. Secreted osteopontin from CD4Cell reports · 2021
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  12. Review
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  14. Review
  15. Osteopontin in Vascular Disease.Arteriosclerosis, thrombosis, and vascular biology · 2019
    Article
  16. Bioscience reports · 2019
    Article
  17. Article
  18. Article
  19. Article
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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

15 authors at 4 institutions in 3 countries.

Katja HeilmannMedical Clinic, Charité University Medicine Berlin, Germany.
Ute Hoffmann
Ellen Witte
Christoph Loddenkemper
Christian Sina
Stefan Schreiber
Claudia Hayford
Pamela Holzlöhner
Kerstin Wolk
Elianne Tchatchou
Verena Moos
Martin Zeitz
Robert Sabat
Ursula Günthert
Bianca Maria Wittig
Charité - Universitätsmedizin Berlin · DEUniversity Hospital of Basel · CHUniversity Hospital Schleswig-Holstein · DEUniversity of Lübeck · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Osteopontin (OPN) is characterized as a major amplifier of Th1-immune responses. However, its role in intestinal inflammation is currently unknown. We found considerably raised OPN levels in blood of wild-type (WT) mice with dextran sodium sulfate (DSS)-induced colitis. To identify the role of this mediator in intestinal inflammation, we analysed experimental colitis in OPN-deficient (OPN(-/-)) mice. In the acute phase of colitis these mice showed more extensive colonic ulcerations and mucosal destruction than WT mice, which was abrogated by application of soluble OPN. Within the OPN(-/-) mice, infiltrating macrophages were not activated and showed impaired phagocytosis. Reduced mRNA expression of interleukin (IL)-1 beta and matrix metalloproteinases was found in acute colitis of OPN(-/-) mice. This was associated with decreased blood levels of IL-22, a Th17 cytokine that may mediate epithelial regeneration. However, OPN-(/-) mice showed increased serum levels of tumour necrosis factor (TNF)-alpha, which could be due to systemically present lipopolysaccharide translocated to the gut. In contrast to acute colitis, during chronic DSS-colitis, which is driven by a Th1 response of the lamina propria infiltrates, OPN(-/-) mice were protected from mucosal inflammation and demonstrated lower serum levels of IL-12 than WT mice. Furthermore, neutralization of OPN in WT mice abrogated colitis. Lastly, we demonstrate that in patients with active Crohn's disease OPN serum concentration correlated significantly with disease activity. Taken together, we postulate a dual function of OPN in intestinal inflammation: During acute inflammation OPN seems to activate innate immunity, reduces tissue damage and initiates mucosal repair whereas during chronic inflammation it promotes the Th1 response and strengthens inflammation.

Indexed as

Acute DiseaseAdolescentAdultAgedAnimalsColitisCrohn DiseaseCytokinesDextran SulfateEnzyme-Linked Immunosorbent AssayHumansImmunohistochemistryInflammatory Bowel DiseasesMacrophage ActivationMacrophagesMiceCytokinesDextran SulfateOsteopontin

Identifiers

PMID18627421
PMCPMC4496111
OpenAlexW2029710444

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.