Evidence map›Paper›PMID 41198388›Full record

ArticleThe European respiratory journal2026

Leukocytic ADAM10 and ADAM17 modulate disease severity and systemic outcome in bacterial and viral pneumonia.

Ahmad Aljohmani, Christian Herr, Martin Witzenrath, Linda Pätzold, Markus Bischoff, Philipp Wartenberg, Ulrich Boehm, Christoph Beisswenger, Qinghai Tian, Matthias W Laschke and 5 more

Abstract read
In one paragraph

Article in The European respiratory journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. 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

15 authors.

Ahmad AljohmaniDept of Molecular Pharmacology and Center for Human and Molecular Biology (ZHMB), Saarland University, Homburg, Germany.ORCID https://orcid.org/0000-0003-0982-3583
Christian HerrDept for Internal Medicine V - Pulmonology, Allergology, Intensive Care Medicine, Saarland University, Homburg, Germany.
Martin WitzenrathDept of Infectious Diseases, Respiratory Medicine and Critical Care, Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin, Humboldt-Universität zu Berlin, and Berlin Institute of Health, Berlin, Germany.
Linda PätzoldInstitute for Medical Microbiology and Hygiene, Saarland University, Homburg, Germany.
Markus BischoffInstitute for Medical Microbiology and Hygiene, Saarland University, Homburg, Germany.
Philipp WartenbergCenter for Molecular Signaling (PZMS), and Center for Gender-sensible Biology and Medicine (CGBM), Saarland University, Homburg, Germany.
Ulrich BoehmCenter for Molecular Signaling (PZMS), and Center for Gender-sensible Biology and Medicine (CGBM), Saarland University, Homburg, Germany.
Christoph BeisswengerDept for Internal Medicine V - Pulmonology, Allergology, Intensive Care Medicine, Saarland University, Homburg, Germany.
Qinghai TianInstitute for Molecular Cell Biology, Medical Faculty, Saarland University, Homburg/Saar, Germany.
Matthias W LaschkePharma Science Hub (PSH), Saarland University, Homburg, Germany.
Matthias HannigPharma Science Hub (PSH), Saarland University, Homburg, Germany.
Claus-Michael LehrPharma Science Hub (PSH), Saarland University, Homburg, Germany.
Robert BalsDept for Internal Medicine V - Pulmonology, Allergology, Intensive Care Medicine, Saarland University, Homburg, Germany.ORCID https://orcid.org/0000-0002-1472-9535
Oliver SchillingInstitute for Surgical Pathology, Medical Center - University of Freiburg, Freiburg, Germany.
Daniela YildizDept of Molecular Pharmacology and Center for Human and Molecular Biology (ZHMB), Saarland University, Homburg, Germany daniela.yildiz@uni-saarland.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPneumonia caused by viral or bacterial pathogens such as severe acute respiratory syndrome coronavirus 2 or

methodsThe analysis of coronavirus disease 2019 (COVID-19) and bacterial pneumonia patient samples was combined with

resultsHospitalised bacterial pneumonia and COVID-19 patients displayed a severity dependent increase of ADAM10 and ADAM17 activity on exosomes. These exosomes caused pathophysiological changes of cardiomyocytes and the endothelial barrier. In a pre-clinical murine pneumonia model, we observed that leukocytes contributed to this increase in exosomal proteolytic activity. In the local environment of the lung, ADAM10 orchestrated a pro-inflammatory response with M1 macrophage polarisation, increased reactive oxygen species (ROS) generation, cytokine release, tissue damage and oedema formation, whereas ADAM17 seemed to dampen the initial inflammatory response to an anti-infective, ROS-balanced level.

conclusionLeukocytic ADAM10 and ADAM17 and their release on exosomes may constitute relevant regulatory elements in bacterial and viral pneumonia, with a potential contribution of exosomes to disease progression and systemic inflammatory responses. Therefore, the diagnostic, prognostic and therapeutic value of ADAM10 and ADAM17 should be evaluated in further preclinical and translational studies, addressing the changes of the immune response and exosomes as cargo vehicles both at local site and for the prevention of systemic effects.

Indexed as

ADAM10 ProteinADAM17 ProteinAmyloid Precursor Protein SecretasesCOVID-19LeukocytesPneumonia, BacterialPneumonia, ViralAnimalsDisease Models, AnimalExosomesFemaleHumansMaleMembrane ProteinsMiceMice, KnockoutADAM10 ProteinADAM10 protein, humanAdam10 protein, mouseADAM17 ProteinADAM17 protein, humanAdam17 protein, mouseAmyloid Precursor Protein SecretasesMembrane Proteins

Identifiers

PMID41198388
PMCPMC12917367

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.