Evidence map›Paper›PMID 17205112›Full record

ArticlePloS one2006

Soluble TNF mediates the transition from pulmonary inflammation to fibrosis.

Nikos Oikonomou, Vaggelis Harokopos, Jonathan Zalevsky, Christos Valavanis, Anastasia Kotanidou, David E Szymkowski, George Kollias, Vassilis Aidinis

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
85citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 5% 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

85 citing papers in PubMed, 1 synthesis or guideline pooled it, 135 citations in OpenAlex.

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25 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

8 authors at 4 institutions in 2 countries.

Nikos OikonomouInstitute of Immunology, Biomedical Sciences Research Center Alexander Fleming, Athens, Greece.
Vaggelis Harokopos
Jonathan Zalevsky
Christos Valavanis
Anastasia Kotanidou
David E Szymkowski
George Kollias
Vassilis Aidinis
Alexander Fleming Biomedical Sciences Research Center · GRXencor (United States) · USMetaxa Hospital · GRNational and Kapodistrian University of Athens · GR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundFibrosis, the replacement of functional tissue with excessive fibrous tissue, can occur in all the main tissues and organ systems, resulting in various pathological disorders. Idiopathic Pulmonary Fibrosis is a prototype fibrotic disease involving abnormal wound healing in response to multiple sites of ongoing alveolar epithelial injury. METHODOLOGY/PRINCIPAL

findingsTo decipher the role of TNF and TNF-mediated inflammation in the development of fibrosis, we have utilized the bleomycin-induced animal model of Pulmonary Fibrosis and a series of genetically modified mice lacking components of TNF signaling. Transmembrane TNF expression is shown to be sufficient to elicit an inflammatory response, but inadequate for the transition to the fibrotic phase of the disease. Soluble TNF expression is shown to be crucial for lymphocyte recruitment, a prerequisite for TGF-b1 expression and the development of fibrotic lesions. Moreover, through a series of bone marrow transfers, the necessary TNF expression is shown to originate from the non-hematopoietic compartment further localized in apoptosing epithelial cells.

conclusionsThese results suggest a primary detrimental role of soluble TNF in the pathologic cascade, separating it from the beneficial role of transmembrane TNF, and indicate the importance of assessing the efficacy of soluble TNF antagonists in the treatment of Idiopathic Pulmonary Fibrosis.

Indexed as

AnimalsBleomycinBone Marrow TransplantationDisease Models, AnimalHumansIdiopathic Pulmonary FibrosisInflammationLymphocytesMiceMice, Inbred C57BLMice, KnockoutPulmonary FibrosisReceptors, Tumor Necrosis FactorReceptors, Tumor Necrosis Factor, Type IRNA, MessengerSignal TransductionBleomycinReceptors, Tumor Necrosis FactorReceptors, Tumor Necrosis Factor, Type IRNA, MessengerTnfrh2 protein, mouseTnfrsf1a protein, mouseTransforming Growth Factor beta1Tumor Necrosis Factor-alpha

Identifiers

PMID17205112
PMCPMC1762410
OpenAlexW1994839187

What OpenQuestion holds

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LicenceCC BY
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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.