Evidence mapPaperPMID 40356473Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2025

Characterizing the Emergence of Myeloid-Derived Suppressor Cell Subsets in a Murine Model of Pulmonary Fibrosis.

Nora Vedder, Philipp Gercke, Nikoleta Lautenschlager, Tobias Brunn, Tim Lange, Jakob Schieb, Charlotte Vetter, Chiel van Geffen, Saeed Kolahian

Abstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

9 authors.

Nora VedderGerman Center for Lung Research (DZL), Universities of Giessen and Marburg Lung Center (UGMLC) Philipps University Marburg, Marburg, Germany.
Philipp GerckeGerman Center for Lung Research (DZL), Universities of Giessen and Marburg Lung Center (UGMLC) Philipps University Marburg, Marburg, Germany.
Nikoleta LautenschlagerGerman Center for Lung Research (DZL), Universities of Giessen and Marburg Lung Center (UGMLC) Philipps University Marburg, Marburg, Germany.
Tobias BrunnGerman Center for Lung Research (DZL), Universities of Giessen and Marburg Lung Center (UGMLC) Philipps University Marburg, Marburg, Germany.
Tim LangeGerman Center for Lung Research (DZL), Universities of Giessen and Marburg Lung Center (UGMLC) Philipps University Marburg, Marburg, Germany.
Jakob SchiebGerman Center for Lung Research (DZL), Universities of Giessen and Marburg Lung Center (UGMLC) Philipps University Marburg, Marburg, Germany.
Charlotte VetterGerman Center for Lung Research (DZL), Universities of Giessen and Marburg Lung Center (UGMLC) Philipps University Marburg, Marburg, Germany.
Chiel van GeffenGerman Center for Lung Research (DZL), Universities of Giessen and Marburg Lung Center (UGMLC) Philipps University Marburg, Marburg, Germany.
Saeed KolahianGerman Center for Lung Research (DZL), Universities of Giessen and Marburg Lung Center (UGMLC) Philipps University Marburg, Marburg, Germany.ORCID https://orcid.org/0000-0003-4096-6910

Funding

Deutsche Forschungsgemeinschaft (DFG) 519089268Deutsche Zentrum für Lungenforschung 82DZL005B2Stiftung für Pathobiochemie und Molekulare Diagnostik (Foundation for Pathobiochemistry and Molecular Diagnostics)
6 · The paper itself

Abstract

The immune system plays a major role in pulmonary fibrosis (PF), a devastating lung disease with limited treatment options. Myeloid-derived suppressor cells (MDSCs) are immune cells with remarkable immunosuppressive functions. We hypothesized that their anti-inflammatory activity may dampen PF by inhibiting inflammation and its transition to fibrosis. Here, we studied the emergence of both polymorphonuclear (PMN)- and monocytic (M)-MDSCs in a murine model of PF. We assessed immunological, histopathological, and clinical changes at days 3, 7, 14, and 21 following bleomycin challenge. A comprehensive overview of the role of MDSCs during the acute lung injury and chronic phase of pulmonary fibrosis is provided, along with the effects of MDSCs adoptive transfer and depletion. Inflammation and fibrosis increased over a period of 21 days after bleomycin administration. In the lung, the number of PMN-MDSCs increased, while M-MDSCs decreased over the time following bleomycin challenge. Especially, M-MDSCs showed enhanced suppressive activity on day 3 following bleomycin challenge. Adoptive transfer of PMN-MDSCs attenuated inflammation and fibrosis development. However, depletion of PMN-MDSCs did not lead to an exacerbation of PF. Our results suggest that adoptive transfer of PMN-MDSCs can ameliorate the inflammatory responses and thus the development of fibrosis in a bleomycin-induced pulmonary fibrosis model.

Indexed as

Myeloid-Derived Suppressor CellsPulmonary FibrosisAdoptive TransferAnimalsBleomycinDisease Models, AnimalInflammationLungMaleMiceMice, Inbred C57BLNeutrophilsBleomycinanimal modelfibrosisinflammationmyeloid‐derived suppressor cellspulmonary fibrosis

Identifiers

PMID40356473
PMCPMC12070151

What Socratic holds

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Registered trials

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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 Socratic graph.