Evidence map›Paper›PMID 16026015›Full record

ArticleLung

Oxidized phosphatidylcholine in alveolar macrophages in idiopathic interstitial pneumonias.

N Yoshimi, Y Ikura, Y Sugama, S Kayo, M Ohsawa, S Yamamoto, Y Inoue, K Hirata, H Itabe, J Yoshikawa and 1 more

Abstract read
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In one paragraph

Article in Lung. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Degradation of oxidized phospholipids by lysosomal phospholipase A2 regulates pulmonary fibrosis.American journal of physiology. Lung cellular and molecular physiology · 2025
    Article
  2. Review
  3. Advances in the Protective Mechanism of NO, HFrontiers in cardiovascular medicine · 2020
    Review
  4. Article
  5. Article
  6. Review
  7. A pneumocyte-macrophage paracrine lipid axis drives the lung toward fibrosis.American journal of respiratory cell and molecular biology · 2015
    Article
  8. Review
  9. Article
  10. Suppression of Toll-like receptor 4 activation by endogenous oxidized phosphatidylcholine, KOdiA-PC by inhibiting LPS binding to MD2.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2013
    Article
  11. Article
  12. Effect of oxidized phosphatidylcholine on biomarkers of oxidative stress in rats.Indian journal of clinical biochemistry : IJCB · 2011
    Article
  13. Review
  14. Article
  15. Oxidized phospholipids in control of inflammation and endothelial barrier.Translational research : the journal of laboratory and clinical medicine · 2009
    Review
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.

N YoshimiDepartment of Pathology, Osaka City University Graduate School of Medicine, Osaka, Japan.
Y Ikura
Y Sugama
S Kayo
M Ohsawa
S Yamamoto
Y Inoue
K Hirata
H Itabe
J Yoshikawa
M Ueda

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It has been suggested that oxidative stress plays a pathogenic role in idiopathic interstitial pneumonias. Macrophage- or neutrophil-derived oxidants seem to be important sources of oxidative stress in this group of inflammatory disorders. Recent experimental studies have revealed that oxidative injury during inflammation or apoptosis can change phosphatidylcholine of cell membrane into its oxidized form, which serves as a ligand for macrophage scavenger receptor CD36. Recently, we developed a monoclonal antibody against oxidized phosphatidylcholine. Using this novel antibody, we performed an immunohistochemical investigation to clarify the localization of oxidized phosphatidylcholine in lung tissues of idiopathic interstitial pneumonias and a relationship between oxidized phosphatidylcholine localization and CD36 expression. Lung specimens obtained from patients with desquamative (n = 8) or usual interstitial pneumonia (n = 15) were studied. Thirteen normal lung tissues were also examined as controls. Antibodies against oxidized phosphatidylcholine, CD36, epithelial cells, macrophages, and neutrophils were used as primary antibodies. The positive cell number was counted by computer-aided morphometry. While there were no oxidized phosphatidylcholine-positive cells in normal lungs, lungs of desquamative or usual interstitial pneumonia contained large numbers of oxidized phosphatidylcholine-positive cells in the alveolar spaces. Double-staining analysis revealed that most oxidized phosphatidylcholine-positive cells were macrophages. The oxidized phosphatidylcholine-positive cells were increased in association with the increase in the densities of macrophages (Rs = 0.87, p < 0.0001) and neutrophils (Rs = 0.89, p < 0.0001). Accumulated macrophages also showed distinct CD36 expression. These findings suggest that oxidative stress and the related product, oxidized phosphatidylcholine, play an important role in the pathophysiology of idiopathic interstitial pneumonias.

Indexed as

AgedFemaleHumansImmunohistochemistryLung Diseases, InterstitialMacrophages, AlveolarMaleMiddle AgedOxidative StressPhosphatidylcholinesPulmonary AlveoliPhosphatidylcholines

Identifiers

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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.