Evidence map›Paper›PMID 42343418›Full record

ArticleCell communication and signaling : CCS2026

Bacterial extracellular vesicles modulate epithelial antiviral responses via macrophage-mediated immunomodulation.

Jeff Bierwagen, Mosche Lückhof, Miriam Ruth Heindl, Eva Böttcher-Friebertshäuser, Christoph Rummel, Mareike Lehmann, Bernd Schmeck, Anna Lena Jung

Abstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2026. 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

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

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

8 authors.

Jeff BierwagenInstitute for Lung Research, Universities of Giessen and Marburg Lung Center, Philipps-University Marburg, German Center for Lung Research (DZL), Marburg, Germany.
Mosche LückhofInstitute for Lung Research, Universities of Giessen and Marburg Lung Center, Philipps-University Marburg, German Center for Lung Research (DZL), Marburg, Germany.
Miriam Ruth HeindlInstitute of Virology, Philipps-University Marburg, Marburg, Germany.
Eva Böttcher-FriebertshäuserInstitute of Virology, Philipps-University Marburg, Marburg, Germany.
Christoph RummelDepartment of Veterinary Physiology and Biochemistry, Justus Liebig University Giessen, Giessen, Germany.
Mareike LehmannInstitute for Lung Research, Universities of Giessen and Marburg Lung Center, Philipps-University Marburg, German Center for Lung Research (DZL), Marburg, Germany.
Bernd SchmeckInstitute for Lung Research, Universities of Giessen and Marburg Lung Center, Philipps-University Marburg, German Center for Lung Research (DZL), Marburg, Germany.
Anna Lena JungInstitute for Lung Research, Universities of Giessen and Marburg Lung Center, Philipps-University Marburg, German Center for Lung Research (DZL), Marburg, Germany. anna.jung@uni-marburg.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Bacterial extracellular vesicles (bEVs) are nano-sized, mostly spherical, double-membrane structures secreted by bacteria throughout their life cycle. In addition to their role in many prokaryotic processes, they can interact with cells of the host immune system, enabling a potential for medical application. This study investigated how bEVs from various pathogenic bacteria modulate human macrophage immune responses and their subsequent ability to protect lung alveolar epithelial cells against SARS-CoV-2 infection.Primary human blood-derived macrophages were stimulated with bEVs derived from Legionella pneumophila (Lp), Klebsiella pneumoniae (Kp), Escherichia coli (Ec), Salmonella Typhimurium (Sal) and Streptococcus pneumoniae (Sp). bEVs from Kp, Ec and Sal strongly induced pro-inflammatory cytokines and interferon-stimulated genes via Toll-like receptor 4-dependent signaling. In contrast, bEVs from Lp or Sp elicited minimal or no immune response. Conditioned media from Kp-, Ec- or Sal- bEV-stimulated macrophages further influenced Calu-3 epithelial cells, leading to the induction of interferon-stimulated genes. Notably, SARS-CoV-2 propagation tended to be reduced in Calu-3 cells pre-stimulated with conditioned media from Kp-bEV- and Ec-bEV-treated macrophages, as demonstrated by decreased infectious virus titers in TCID

Indexed as

BacteriaEpithelial CellsExtracellular VesiclesImmunomodulationMacrophagesCOVID-19CytokinesHumansSARS-CoV-2CytokinesBacterial extracellular vesicles (bEVs)Host-pathogen interactionHuman macrophagesInnate immune responsePulmonary infectionSARS-CoV-2Toll-like receptor 4 (TLR4)

Identifiers

PMID42343418
PMCPMC13292577

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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 OpenQuestion graph.