Evidence map›Paper›PMID 26618925›Full record

ArticlePloS one2015

Loss of Ifnar1 in Pancreatic Acinar Cells Ameliorates the Disease Course of Acute Pancreatitis.

Katharina J Miller, Susanne Raulefs, Bo Kong, Katja Steiger, Ivonne Regel, Andreas Gewies, Jörg Kleeff, Christoph W Michalski

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 40% 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

1 citing paper in PubMed, 4 citations in OpenAlex.

  1. 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

8 authors at 2 institutions in 1 country.

Katharina J MillerDepartment of Surgery, Technische Universität München, Munich, Germany.
Susanne RaulefsDepartment of Surgery, Technische Universität München, Munich, Germany.
Bo KongDepartment of Surgery, Technische Universität München, Munich, Germany.
Katja SteigerInstitute of Pathology, Technische Universität München, Munich, Germany.
Ivonne RegelDepartment of Surgery, Technische Universität München, Munich, Germany.
Andreas GewiesInstitute für Klinische Chemie und Pathobiochemie, Technische Universität München, Munich, Germany.
Jörg KleeffDepartment of Surgery, Technische Universität München, Munich, Germany.
Christoph W MichalskiDepartment of Surgery, University Hospital Heidelberg, Heidelberg, Germany.
Technical University of Munich · DEUniversity Hospital Heidelberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type I interferon constitutes an essential component of the combinational therapy against viral disease. Acute pancreatitis is one side effect of type I interferon-based therapy, implying that activation of type I interferon signaling affects the homeostasis and integrity of pancreatic acinar cells. Here, we investigated the role of type I interferon signaling in pancreatic acinar cells using a caerulein-induced murine model of acute pancreatitis. Pancreas-specific ablation of interferon (alpha and beta) receptor 1 (Ifnar1) partially protected animals from caerulein-induced pancreatitis, as demonstrated by reduced tissue damage. Profiling of infiltrating immune cells revealed that this dampened tissue damage response correlated with the number of macrophages in the pancreas. Pharmacologic depletion of macrophages reversed the protective effect of Ifnar1 deficiency. Furthermore, expression of chemokine (C-C motif) ligand 2 (Ccl2), a potent factor for macrophage recruitment, was significantly increased in the Ifnar1-deficient pancreas. Thus, type I interferon signaling in pancreatic acinar cells controls pancreatic homeostasis by affecting the macrophage-mediated inflammatory response in the pancreas.

Indexed as

Acinar CellsAnimalsChemokine CCL2MacrophagesMiceMice, Inbred C57BLPancreatitis, Acute NecrotizingReceptor, Interferon alpha-betaChemokine CCL2Ifnar1 protein, mouseReceptor, Interferon alpha-beta

Identifiers

PMID26618925
PMCPMC4664425
OpenAlexW2189250150

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.