Evidence map›Paper›PMID 24150257›Full record

ReviewMucosal immunology2014

DAMPs activating innate and adaptive immune responses in COPD.

S D Pouwels, I H Heijink, N H T ten Hacken, P Vandenabeele, D V Krysko, M C Nawijn, A J M van Oosterhout

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Mucosal immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.

0numbers the graph read from it
0cells of the map it votes in
110citing papers in PubMed
14.7field-weighted citation impact, top 1% 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

110 citing papers in PubMed, 175 citations in OpenAlex.

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  12. CD207-Positive Dendritic Cells Promote Emphysema Through CD8Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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50 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

7 authors at 3 institutions in 2 countries.

S D Pouwels1] Department of Pathology and Medical Biology, Laboratory of Allergology and Pulmonary Diseases, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands [2] GRIAC Research Institute, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
I H Heijink1] Department of Pathology and Medical Biology, Laboratory of Allergology and Pulmonary Diseases, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands [2] GRIAC Research Institute, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
N H T ten Hacken1] GRIAC Research Institute, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands [2] Department of Pulmonary Disease, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
P Vandenabeele1] Molecular Signaling and Cell Death Unit, Department for Molecular Biomedical Research, VIB, Ghent, Belgium [2] Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.
D V Krysko1] Molecular Signaling and Cell Death Unit, Department for Molecular Biomedical Research, VIB, Ghent, Belgium [2] Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium.
M C Nawijn1] Department of Pathology and Medical Biology, Laboratory of Allergology and Pulmonary Diseases, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands [2] GRIAC Research Institute, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
A J M van Oosterhout1] Department of Pathology and Medical Biology, Laboratory of Allergology and Pulmonary Diseases, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands [2] GRIAC Research Institute, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
University of Groningen · NLGhent University · BEUniversity Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic obstructive pulmonary disease (COPD), a progressive lung disease characterized by sustained neutrophilic airway inflammation, is caused by chronic exposure to noxious stimuli, e.g., cigarette smoke. This chronic exposure can induce immunogenic cell death of structural airway cells, inducing the release of damage-associated molecular patterns (DAMPs). Levels of several DAMPs, including S100 proteins, defensins, and high-mobility group box-1 (HMGB1), are increased in extracellular lung fluids of COPD patients. As DAMPs can attract and activate immune cells upon binding to pattern recognition receptors, we propose that their release may contribute to neutrophilic airway inflammation. In this review, we discuss the novel role of DAMPs in COPD pathogenesis. Relevant DAMPs are categorized based on their subcellular origin, i.e. cytoplasm, endoplasmic reticulum, nucleus, and mitochondria. Furthermore, their potential role in the pathophysiology of COPD will be discussed.

Indexed as

Adaptive ImmunityImmunity, InnateAnimalsCarrier ProteinsExtracellular SpaceHumansIntracellular SpaceProtein BindingPulmonary Disease, Chronic ObstructiveReceptors, Pattern RecognitionSignal TransductionCarrier ProteinsReceptors, Pattern Recognition

Identifiers

PMID24150257
OpenAlexW1989289468

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.