Evidence map›Paper›PMID 29649237›Full record

ArticlePloS one2018

Bronchoalveolar lavage (BAL) cells in idiopathic pulmonary fibrosis express a complex pro-inflammatory, pro-repair, angiogenic activation pattern, likely associated with macrophage iron accumulation.

Jungnam Lee, Ivan Arisi, Ermanno Puxeddu, Lazarus K Mramba, Massimo Amicosante, Carmen M Swaisgood, Marco Pallante, Mark L Brantly, C Magnus Sköld, Cesare Saltini

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
5.1field-weighted citation impact, top 4% of its field
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

44 citing papers in PubMed, 67 citations in OpenAlex.

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  2. Regulated Cell Death in Idiopathic Pulmonary Fibrosis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 4 institutions in 3 countries.

Jungnam LeeDivision of Pulmonary, Critical Care and Sleep Medicine, University of Florida College of Medicine, Gainesville, Florida, United States of America.
Ivan ArisiGenomics Facility, European Brain Research Institute, Rome, Italy.
Ermanno PuxedduDepartment of Biomedicine and Prevention, University of Roma "Tor Vergata", Rome, Italy.
Lazarus K MrambaDepartment of Medicine, University of Florida College of Medicine, Gainesville, Florida, United States of America.
Massimo AmicosanteDepartment of Biomedicine and Prevention, University of Roma "Tor Vergata", Rome, Italy.
Carmen M SwaisgoodDivision of Pulmonary, Critical Care and Sleep Medicine, University of Florida College of Medicine, Gainesville, Florida, United States of America.
Marco PallanteDepartment of Biomedicine and Prevention, University of Roma "Tor Vergata", Rome, Italy.
Mark L BrantlyDivision of Pulmonary, Critical Care and Sleep Medicine, University of Florida College of Medicine, Gainesville, Florida, United States of America.
C Magnus SköldDepartment of Medicine, Respiratory Medicine Unit, and Lung-Allergy Clinic, Karolinska University Hospital Solna, Stockholm, Sweden.
Cesare SaltiniDivision of Pulmonary, Critical Care and Sleep Medicine, University of Florida College of Medicine, Gainesville, Florida, United States of America.ORCID 0000-0002-8976-4917
University of Florida · USUniversity of Rome Tor Vergata · ITEuropean Brain Research Institute · ITKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Idiopathic pulmonary fibrosis (IPF) is a chronic lung disease of unknown cause characterized by alveolar epithelial damage, patchy interstitial fibrosis and diffuse microvascular abnormalities. In IPF, alveolar clustering of iron-laden alveolar macrophages-a common sign of microhemorrhage, has been associated with vascular abnormalities and worsening of pulmonary hypertension. As iron-dependent ROS generation has been shown to induce unrestrained macrophage activation in disease models of vascular damage, we explored alveolar macrophage activation phenotype in IPF patients (n = 16) and healthy controls (CTR, n = 7) by RNA sequencing of bronchoalveolar lavage (BAL) cells. The frequencies of macrophages in BAL cells were 86+4% and 83.4+8% in IPF and CTR groups, respectively (p-value = 0.41). In IPF patients, BAL cells showed increased iron-dependent ROS generation (p-value<0.05 vs CTR). Gene expression analysis showed overrepresentation of Gene Ontology processes/functions and KEGG pathways enriched in upregulated M1-type inflammatory (p-value<0.01), M2-type anti-inflammatory/tissue remodeling (p-value<0.0001), and MTPP-type chronic inflammatory/angiogenic (p-value<0.0001) chemokine and cytokine genes. The ex vivo finding was confirmed by the induction of iron-dependent ROS generation and chemokine/cytokine overexpression of Ccl4, Cxcl10 (M1), Il1rn (M2), Cxcl2, and Cxcl7 (MTPP) in MH-S murine immortalized alveolar macrophages exposed to ferric ammonium citrate in culture (p-value<0.05 vs CTR). The data show alveolar macrophage expression of a pro-inflammatory, tissue remodeling and angiogenic complex activation pattern, suggesting that iron accumulation may play a role in macrophage activation.

Indexed as

Neovascularization, PathologicAdultAgedBronchoalveolar Lavage FluidChemokinesFemaleGene Expression ProfilingHumansIdiopathic Pulmonary FibrosisInflammationIronMacrophagesMaleMiddle AgedPhenotypeReactive Oxygen SpeciesChemokinesIronReactive Oxygen Species

Identifiers

PMID29649237
PMCPMC5896901
OpenAlexW2798081375

What OpenQuestion holds

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LicenceCC BY
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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.