Evidence map›Paper›PMID 41202119›Full record

ArticleScience advances2025

Alveolar macrophages initiate the spatially targeted recruitment of neutrophils after nanoparticle inhalation.

Qiongliang Liu, Lin Yang, Chenxi Li, Lianyong Han, Juliet Wilmot, Guo Yang, Riccardo Leinardi, Qiaoxia Zhou, Andreas Schröppel, David Kutschke and 9 more

Abstract read
In one paragraph

Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Prophylactic immune priming with heat-killedFrontiers in immunology · 2026
    Article
  2. Review
  3. Readiness of theFrontiers in toxicology · 2026
    Article
  4. Review
  5. Article
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

19 authors.

Qiongliang LiuInstitute of Lung Health and Immunity (LHI), Comprehensive Pneumology Center (CPC), Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.ORCID 0009-0000-6113-6057
Lin YangInstitute of Lung Health and Immunity (LHI), Comprehensive Pneumology Center (CPC), Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.
Chenxi LiInstitute of Lung Health and Immunity (LHI), Comprehensive Pneumology Center (CPC), Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.
Lianyong HanInstitute of Lung Health and Immunity (LHI), Comprehensive Pneumology Center (CPC), Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.ORCID 0000-0001-8623-776X
Juliet WilmotLouvain Center for Toxicology and Applied Pharmacology (LTAP), Institut de Recherche Expérimental et Clinique (IREC), Université Catholique de Louvain, Louvain-la-Neuve, Belgium.
Guo YangInstitute of Lung Health and Immunity (LHI), Comprehensive Pneumology Center (CPC), Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.
Riccardo LeinardiLouvain Center for Toxicology and Applied Pharmacology (LTAP), Institut de Recherche Expérimental et Clinique (IREC), Université Catholique de Louvain, Louvain-la-Neuve, Belgium.
Qiaoxia ZhouInstitute of Lung Health and Immunity (LHI), Comprehensive Pneumology Center (CPC), Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.
Andreas SchröppelInstitute of Lung Health and Immunity (LHI), Comprehensive Pneumology Center (CPC), Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.
David KutschkeInstitute of Lung Health and Immunity (LHI), Comprehensive Pneumology Center (CPC), Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.ORCID 0009-0002-0154-2357
Judith SecklehnerCancer Research UK Scotland Institute, Glasgow, UK.ORCID 0000-0003-0005-3535
Ali Önder YldirimInstitute of Lung Health and Immunity (LHI), Comprehensive Pneumology Center (CPC), Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.ORCID 0000-0003-1969-480X
François HuauxLouvain Center for Toxicology and Applied Pharmacology (LTAP), Institut de Recherche Expérimental et Clinique (IREC), Université Catholique de Louvain, Louvain-la-Neuve, Belgium.
Dagmar ZeuschnerElectron Microscopy Facility, Max Planck Institute for Molecular Biomedicine, Muenster, Germany.
Leo M CarlinCancer Research UK Scotland Institute, Glasgow, UK.ORCID 0000-0001-7172-5234
Markus SperandioWalter Brendel Centre of Experimental Medicine, Biomedical Center, Institute of Cardiovascular Physiology and Pathophysiology, Ludwig-Maximilians-Universität München, Planegg-Martinsried, Germany.ORCID 0000-0002-7689-3613
Otmar SchmidInstitute of Lung Health and Immunity (LHI), Comprehensive Pneumology Center (CPC), Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.ORCID 0000-0002-8012-7786
Tobias StoegerInstitute of Lung Health and Immunity (LHI), Comprehensive Pneumology Center (CPC), Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.ORCID 0000-0002-2790-0389
Markus RehbergInstitute of Lung Health and Immunity (LHI), Comprehensive Pneumology Center (CPC), Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.ORCID 0000-0001-7314-6332

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lung resident immune cells are essential for initiating defenses against inhaled air pollutants, including nanoparticles (NPs), which contribute to pulmonary disease progression. Here, lung intravital microscopy was used to examine the pulmonary innate immune responses in mice, during acute aerosol exposure to carbon NPs, a common environmental pollutant, or fluorescent quantum dot NPs. We found that inhaled NPs triggered rapid, neutrophil recruitment, localized to alveolar NP deposition hotspots, orchestrated by alveolar macrophages (AMs) through both their motility and phagocytic activity. AM motility inhibition in the alveoli via intercellular adhesion molecule-1/LFA-1 blockade reduced neutrophil recruitment, as did impaired AM phagocytosis through C5a receptor 1/Fc-γ receptor I inhibition or by stealth NP surfaces. In addition, cellular degranulation inhibition indicated the importance of spatially focused cytokine release in neutrophil recruitment. Collectively, our study elucidates AM-epithelial interactions as a critical key event for NPs triggered neutrophilia, with AM motility and phagocytosis driving recruitment and site-specific immune responses in the alveolar microenvironment.

Indexed as

Macrophages, AlveolarNanoparticlesNeutrophil InfiltrationNeutrophilsAnimalsCell MovementMiceMice, Inbred C57BLPhagocytosis

Identifiers

PMID41202119
PMCPMC12594175

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.