Evidence map›Paper›PMID 16412062›Full record

ArticleClinical and experimental immunology2006

Alveolar macrophage function is altered in patients with lung cancer.

D S Pouniotis, M Plebanski, V Apostolopoulos, C F McDonald

Open access · greenAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.6field-weighted citation impact, top 33% 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

21 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
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  10. Article
  11. Expression ofTranslational cancer research · 2020
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Alveolar Macrophage Polarisation in Lung Cancer.Lung cancer international · 2014
    Review
  20. [HLA and immune of lung cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2010
    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

4 authors at 1 institution in 1 country.

D S PouniotisImmunology and Vaccine Laboratory, Austin Research Institute, Heidelberg, Victoria, Australia.
M Plebanski
V Apostolopoulos
C F McDonald
Austin Health · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The alveolar macrophage (AM) is believed to be of central importance in the immune response against infection and tumour. We examined patients with lung cancer in order to evaluate the immuno-stimulatory potential of AM in lung cancer. Bronchoalveolar lavage fluid samples were obtained from patients with adenocarcinoma, squamous cell carcinoma, large cell undifferentiated lung carcinoma, small cell carcinoma and control subjects. AM were isolated and phagocytic function, flow cytometry and cytokine analysis were assessed. AM from patients with small and squamous cell carcinoma had impaired uptake in vitro of 40 nm fluorescent polystyrene beads. AM from patients with small, squamous and large cell undifferentiated carcinoma showed impaired uptake of 1000 nm fluorescent polystyrene beads. Secreted levels of TNF-alpha and IL-1 from AM of patients with small, squamous, and large cell undifferentiated carcinoma were decreased compared to controls. Secreted AM IL-6 levels were decreased in small and large cell undifferentiated carcinoma. AM from adenocarcinoma patients showed similar levels of IL-10, IL-6, IL-1 and TNF-alpha compared to controls. Phenotypic analysis demonstrated that patients with small cell carcinoma were the only group that showed a decrease in MHC class II surface expression. Surface expression of ICAM-1 and CD83 was decreased on AM from patients with large, squamous and small cell carcinoma compared to controls but not adenocarcinoma. Mannose receptor levels were only decreased on AM from patients with squamous and small cell carcinoma but not adenocarcinoma and large cell undifferentiated carcinoma. We conclude that there are type-specific alterations in uptake ability, cytokine secretion and phenotype of AM from lung cancer patients, which may result in an inability to stimulate anti-tumour immunity. The observed differences between lung cancer subgroups may explain previously reported inconsistencies in descriptions of AM characteristics in lung cancer.

Indexed as

AdenocarcinomaAgedAntigens, CDBiomarkersBronchoalveolar Lavage FluidCarcinoma, Large CellCarcinoma, Small CellCarcinoma, Squamous CellCD83 AntigenCytokinesHLA-DR AntigensHumansImmunoglobulinsIntercellular Adhesion Molecule-1Lectins, C-TypeLung NeoplasmsAntigens, CDBiomarkersCD83 AntigenCytokinesHLA-DR AntigensImmunoglobulinsIntercellular Adhesion Molecule-1Lectins, C-TypeMannose-Binding LectinsMannose ReceptorMembrane GlycoproteinsPolystyrenesReceptors, Cell Surface

Identifiers

PMID16412062
PMCPMC1809587
OpenAlexW2067739241

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.