Evidence map›Paper›PMID 24828408›Full record

ArticlePloS one2014

Mononuclear phagocytes and airway epithelial cells: novel sources of matrix metalloproteinase-8 (MMP-8) in patients with idiopathic pulmonary fibrosis.

Vanessa J Craig, Francesca Polverino, Maria E Laucho-Contreras, Yuanyuan Shi, Yushi Liu, Juan C Osorio, Yohannes Tesfaigzi, Victor Pinto-Plata, Bernadette R Gochuico, Ivan O Rosas and 1 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

25 citing papers in PubMed, 61 citations in OpenAlex.

  1. A bioengineered living cell construct activates metallothionein/zinc/MMP8 and inhibits TGFβ to stimulate remodeling of fibrotic venous leg ulcers.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2020
    Trial
  2. Matrix Metalloproteinase-8 Deficiency Alters the Balance Between Viral Clearance and Immunopathology in H1N1 Infection.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  3. The Immune Microenvironment: New Therapeutic Implications in Organ Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
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  17. Unraveling the ECM-Immune Cell Crosstalk in Skin Diseases.Frontiers in cell and developmental biology · 2019
    Review
  18. Cigarette smoke exposure worsens acute lung injury in antibiotic-treated bacterial pneumonia in mice.American journal of physiology. Lung cellular and molecular physiology · 2018
    Article
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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

11 authors at 4 institutions in 2 countries.

Vanessa J CraigDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
Francesca PolverinoDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America; Department of Clinical and Experimental Medicine, University of Parma, Parma, Italy; Pulmonary Fibrosis Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico, United States of America.
Maria E Laucho-ContrerasDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
Yuanyuan ShiDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America; Pulmonary Fibrosis Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico, United States of America.
Yushi LiuDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America; Pulmonary Fibrosis Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico, United States of America.
Juan C OsorioDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
Yohannes TesfaigziChronic Obstructive Pulmonary Disease Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico, United States of America.
Victor Pinto-PlataDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America.
Bernadette R GochuicoMedical Genetics Branch, National Human Genome Research Institute, National Institutes of Health, Bethesda, Maryland, United States of America.
Ivan O RosasDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America; Pulmonary Fibrosis Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico, United States of America.
Caroline A OwenDivision of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, United States of America; Pulmonary Fibrosis Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico, United States of America; Chronic Obstructive Pulmonary Disease Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico, United States of America.
Lovelace Respiratory Research Institute · USHarvard University · USBrigham and Women's Hospital · USNational Institutes of Health · US

Funding

Respiratory Computational Discovery CoreP01HL114501 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI CHOI, MARY E · 2013 to 2025
$24.9M
RESPIRATORY RESEARCHT32HL007633 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI George R Washko · 1985 to 2026
$14.9M
Training Program in Newborn and Developmental DiseasesT32HD007466 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI KOUREMBANAS, STELLA · 1994 to 2016
$8.0M
Novel Roles for MMP-8 in Acute Lung InjuryR01HL063137 · NHLBI · UNIVERSITY OF UTAH · PI OWEN, CAROLINE A · 1999 to 2008
$2.6M
Novel Roles for ADAM15 in Acute Lung InjuryR01HL086814 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI OWEN, CAROLINE A · 2007 to 2010
$1.6M
Novel Anti-inflammatory Activities For ADAM8 In Pulmonary EmphysemaR21HL111835 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI OWEN, CAROLINE A · 2012 to 2013
$456k
NHLBI NIH HHS 2T32 HL007633-26NHLBI NIH HHS HL086814NHLBI NIH HHS HL111835NHLBI NIH HHS HL63137NHLBI NIH HHS P01 HL114501NHLBI NIH HHS R01 HL063137NHLBI NIH HHS R01 HL086814NHLBI NIH HHS R21 HL111835NHLBI NIH HHS T32 HL007633NICHD NIH HHS 5T32 HD007466-15NICHD NIH HHS T32 HD007466
6 · The paper itself

Abstract

objectivesMatrix metalloproteinase-8 (MMP-8) promotes lung fibrotic responses to bleomycin in mice. Although prior studies reported that MMP-8 levels are increased in plasma and bronchoalveolar lavage fluid (BALF) samples from IPF patients, neither the bioactive forms nor the cellular sources of MMP-8 in idiopathic pulmonary fibrosis (IPF) patients have been identified. It is not known whether MMP-8 expression is dys-regulated in IPF leukocytes or whether MMP-8 plasma levels correlate with IPF outcomes. Our goal was to address these knowledge gaps.

methodsWe measured MMP-8 levels and forms in blood and lung samples from IPF patients versus controls using ELISAs, western blotting, and qPCR, and assessed whether MMP-8 plasma levels in 73 IPF patients correlate with rate of lung function decline and mortality. We used immunostaining to localize MMP-8 expression in IPF lungs. We quantified MMP-8 levels and forms in blood leukocytes from IPF patients versus controls.

resultsIPF patients have increased BALF, whole lung, and plasma levels of soluble MMP-8 protein. Active MMP-8 is the main form elevated in IPF lungs. MMP-8 mRNA levels are increased in monocytes from IPF patients, but IPF patients and controls have similar levels of MMP-8 in PMNs. Surprisingly, macrophages and airway epithelial cells are the main cells expressing MMP-8 in IPF lungs. Plasma and BALF MMP-8 levels do not correlate with decline in lung function and/or mortality in IPF patients.

conclusionBlood and lung MMP-8 levels are increased in IPF patients. Active MMP-8 is the main form elevated in IPF lungs. Surprisingly, blood monocytes, lung macrophages, and airway epithelial cells are the main cells in which MMP-8 is upregulated in IPF patients. Plasma and BALF MMP-8 levels are unlikely to serve as a prognostic biomarker for IPF patients. These results provide new information about the expression patterns of MMP-8 in IPF patients.

Indexed as

AgedBronchoalveolar Lavage FluidEpithelial CellsFemaleHumansIdiopathic Pulmonary FibrosisLeukocytesLungMacrophages, AlveolarMaleMatrix Metalloproteinase 8Middle AgedMononuclear Phagocyte SystemMatrix Metalloproteinase 8

Identifiers

PMID24828408
PMCPMC4020836
OpenAlexW2157344181

What OpenQuestion holds

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LicenceCC BY
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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.