Evidence map›Paper›PMID 24901869›Full record

ArticlePloS one2014

Oxidative stress decreases functional airway mannose binding lectin in COPD.

Hai B Tran, Jessica Ahern, Greg Hodge, Phillip Holt, Melinda M Dean, Paul N Reynolds, Sandra Hodge

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 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-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

18 citing papers in PubMed, 40 citations in OpenAlex.

  1. Trial
  2. When clearance fails: the role of efferocytosis in COPD.European respiratory review : an official journal of the European Respiratory Society · 2026
    Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
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  10. Article
  11. Review
  12. Article
  13. Review
  14. Gene expression profile of human lung in a relatively early stage of COPD with emphysema.International journal of chronic obstructive pulmonary disease · 2018
    Article
  15. Article
  16. Review
  17. Article
  18. 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

7 authors at 4 institutions in 1 country.

Hai B TranLung Research, Hanson Institute and Department Thoracic Medicine, Royal Adelaide Hospital, Adelaide, South Australia, Australia.
Jessica AhernLung Research, Hanson Institute and Department Thoracic Medicine, Royal Adelaide Hospital, Adelaide, South Australia, Australia.
Greg HodgeLung Research, Hanson Institute and Department Thoracic Medicine, Royal Adelaide Hospital, Adelaide, South Australia, Australia; Department of Medicine, University of Adelaide, Adelaide, South Australia, Australia.
Phillip HoltLung Research, Hanson Institute and Department Thoracic Medicine, Royal Adelaide Hospital, Adelaide, South Australia, Australia.
Melinda M DeanResearch and Development, Australian Red Cross Blood Service, Brisbane, Queensland, Australia.
Paul N ReynoldsLung Research, Hanson Institute and Department Thoracic Medicine, Royal Adelaide Hospital, Adelaide, South Australia, Australia; Department of Medicine, University of Adelaide, Adelaide, South Australia, Australia.
Sandra HodgeLung Research, Hanson Institute and Department Thoracic Medicine, Royal Adelaide Hospital, Adelaide, South Australia, Australia; Department of Medicine, University of Adelaide, Adelaide, South Australia, Australia.
Royal Adelaide Hospital · AUHanson Institute · AUAustralian Red Cross Lifeblood · AUUniversity of Adelaide · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have previously established that a defect in the ability of alveolar macrophages (AM) to phagocytose apoptotic cells (efferocytosis) and pathogens is a potential therapeutic target in COPD. We further showed that levels of mannose binding lectin (MBL; required for effective macrophage phagocytic function) were reduced in the airways but not circulation of COPD patients. We hypothesized that increased oxidative stress in the airway could be a cause for such disturbances. We therefore studied the effects of oxidation on the structure of the MBL molecule and its functional interactions with macrophages. Oligomeric structure of plasma derived MBL (pdMBL) before and after oxidation (oxMBL) with 2,2'-azobis(2-methylpropionamidine)dihydrochroride (AAPH) was investigated by blue native PAGE. Macrophage function in the presence of pd/oxMBL was assessed by measuring efferocytosis, phagocytosis of non-typeable Haemophilus influenzae (NTHi) and expression of macrophage scavenger receptors. Oxidation disrupted higher order MBL oligomers. This was associated with changed macrophage function evident by a significantly reduced capacity to phagocytose apoptotic cells and NTHi in the presence of oxMBL vs pdMBL (eg, NTHi by 55.9 and 27.0% respectively). Interestingly, oxidation of MBL significantly reduced macrophage phagocytic ability to below control levels. Flow cytometry and immunofluorescence revealed a significant increase in expression of macrophage scavenger receptor (SRA1) in the presence of pdMBL that was abrogated in the presence of oxMBL. We show the pulmonary macrophage dysfunction in COPD may at least partially result from an oxidative stress-induced effect on MBL, and identify a further potential therapeutic strategy for this debilitating disease.

Indexed as

Oxidative StressApoptosisBronchoalveolar Lavage FluidCell LineHumansMacrophages, AlveolarMannose-Binding LectinOxidation-ReductionPhagocytosisPulmonary Disease, Chronic ObstructiveReceptors, ScavengerRespiratory MucosaRespiratory SystemMannose-Binding LectinReceptors, Scavenger

Identifiers

PMID24901869
PMCPMC4047017
OpenAlexW2070429029

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.