Evidence map›Paper›PMID 39478566›Full record

ArticleCritical care (London, England)2024

Airway epithelium damage in acute respiratory distress syndrome.

Ludovic Gerard, Marylene Lecocq, Bruno Detry, Caroline Bouzin, Delphine Hoton, Joao Pinto Pereira, François Carlier, Thomas Plante-Bordeneuve, Sophie Gohy, Valérie Lacroix and 2 more

Abstract read
In one paragraph

Article in Critical care (London, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed.

  1. Diffuse alveolar damage, acute respiratory distress syndrome (ARDS), and non-cardiogenic pulmonary edema. Part 1: ARDS endotypes, including systemic inflammatory response syndrome and sepsis, with dog and cat examples.Journal of veterinary diagnostic investigation : official publication of the American Association of Veterinary Laboratory Diagnosticians, Inc · 2026
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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

12 authors.

Ludovic GerardDepartment of Critical Care Medicine, Cliniques universitaires Saint Luc, Université catholique de Louvain (UCLouvain), Avenue Hippocrate 10, 1200, Brussels, Belgium. ludovic.gerard@saintluc.uclouvain.be.ORCID 0000-0002-8842-6270
Marylene LecocqPôle de Pneumologie, O.R.L. et Dermatologie (LuNS, Lung-Nose-Skin), Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain (UCLouvain), Brussels, Belgium.
Bruno DetryPôle de Pneumologie, O.R.L. et Dermatologie (LuNS, Lung-Nose-Skin), Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain (UCLouvain), Brussels, Belgium.
Caroline BouzinIREC Imaging Platform (2IP, RRID:SCR_023378), Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain (UCLouvain), Brussels, Belgium.
Delphine HotonDepartment of Pathology, Cliniques universitaires Saint Luc, Université catholique de Louvain (UCLouvain), Brussels, Belgium.
Joao Pinto PereiraDepartment of Critical Care Medicine, Cliniques universitaires Saint Luc, Université catholique de Louvain (UCLouvain), Avenue Hippocrate 10, 1200, Brussels, Belgium.
François CarlierPôle de Pneumologie, O.R.L. et Dermatologie (LuNS, Lung-Nose-Skin), Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain (UCLouvain), Brussels, Belgium.
Thomas Plante-BordeneuvePôle de Pneumologie, O.R.L. et Dermatologie (LuNS, Lung-Nose-Skin), Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain (UCLouvain), Brussels, Belgium.
Sophie GohyPôle de Pneumologie, O.R.L. et Dermatologie (LuNS, Lung-Nose-Skin), Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain (UCLouvain), Brussels, Belgium.
Valérie LacroixDepartment of Cardiovascular and Thoracic Surgery, Cliniques universitaires Saint Luc, Université catholique de Louvain (UCLouvain), Brussels, Belgium.
Pierre-François LaterreDepartment of Intensive Care Medicine, Centre Hospitalier Régional Mons-Hainaut, Mons, Belgium.
Charles PilettePôle de Pneumologie, O.R.L. et Dermatologie (LuNS, Lung-Nose-Skin), Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain (UCLouvain), Brussels, Belgium.

Funding

Fonds De La Recherche Scientifique - FNRS 1.R017.18Fonds De La Recherche Scientifique - FNRS 1.R017.20Fonds De La Recherche Scientifique - FNRS F5/4/140/5
6 · The paper itself

Abstract

backgroundThe airway epithelium (AE) fulfils multiple functions to maintain pulmonary homeostasis, among which ensuring adequate barrier function, cell differentiation and polarization, and actively transporting immunoglobulin A (IgA), the predominant mucosal immunoglobulin in the airway lumen, via the polymeric immunoglobulin receptor (pIgR). Morphological changes of the airways have been reported in ARDS, while their detailed features, impact for mucosal immunity, and causative mechanisms remain unclear. Therefore, this study aimed to assess epithelial alterations in the distal airways of patients with ARDS.

methodsWe retrospectively analyzed lung tissue samples from ARDS patients and controls to investigate and quantify structural and functional changes in the small airways, using multiplex fluorescence immunostaining and computer-assisted quantification on whole tissue sections. Additionally, we measured markers of mucosal immunity, IgA and pIgR, alongside with other epithelial markers, in the serum and the broncho-alveolar lavage fluid (BALF) prospectively collected from ARDS patients and controls.

resultsCompared to controls, airways of ARDS were characterized by increased epithelial denudation (p = 0.0003) and diffuse epithelial infiltration by neutrophils (p = 0.0005). Quantitative evaluation of multiplex fluorescence immunostaining revealed a loss of ciliated cells (p = 0.0317) a trend towards decreased goblet cells (p = 0.056), and no change regarding cell progenitors (basal and club cells), indicating altered mucociliary differentiation. Increased epithelial permeability was also shown in ARDS with a significant decrease of tight (p < 0.0001) and adherens (p = 0.025) junctional proteins. Additionally, we observed a significant decrease of the expression of pIgR, (p < 0.0001), indicating impaired mucosal IgA immunity. Serum concentrations of secretory component (SC) and S-IgA were increased in ARDS (both p < 0.0001), along other lung-derived proteins (CC16, SP-D, sRAGE). However, their BALF concentrations remained unchanged, suggesting a spillover of airway and alveolar proteins through a damaged AE.

conclusionThe airway epithelium from patients with ARDS exhibits multifaceted alterations leading to altered mucociliary differentiation, compromised defense functions and increased permeability with pneumoproteinemia.

Indexed as

Respiratory Distress SyndromeAdultAgedBronchoalveolar Lavage FluidFemaleHumansMaleMiddle AgedRespiratory MucosaRetrospective StudiesAirway epitheliumARDSCiliated cellsImmunoglobulin AJunctional proteinsMucosal immunityPneumoproteinemia

Identifiers

PMID39478566
PMCPMC11523598

What OpenQuestion 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 OpenQuestion graph.