Evidence map›Paper›PMID 11122454›Full record

ArticleImmunology2000

A critical role for alveolar macrophages in elicitation of pulmonary immune fibrosis.

J Zhang-Hoover, A Sutton, N van Rooijen, J Stein-Streilein

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2000. 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 29% 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, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Loss of CD73 prevents accumulation of alternatively activated macrophages and the formation of prefibrotic macrophage clusters in irradiated lungs.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017
    Article
  7. Article
  8. A pneumocyte-macrophage paracrine lipid axis drives the lung toward fibrosis.American journal of respiratory cell and molecular biology · 2015
    Article
  9. Association of age-dependent liver injury and fibrosis with immune cell populations.Liver international : official journal of the International Association for the Study of the Liver · 2013
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. The chemokine, CCL3, and its receptor, CCR1, mediate thoracic radiation-induced pulmonary fibrosis.American journal of respiratory cell and molecular biology · 2011
    Article
  15. Article
  16. Abnormal lymphangiogenesis in idiopathic pulmonary fibrosis with insights into cellular and molecular mechanisms.Proceedings of the National Academy of Sciences of the United States of America · 2009
    Article
  17. Article
  18. Article
  19. Impairment of alveolar macrophage transcription in idiopathic pulmonary fibrosis.American journal of respiratory and critical care medicine · 2007
    Article
  20. 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

4 authors at 4 institutions in 2 countries.

J Zhang-HooverSchepens Eye Research Institute, Boston, Massachusetts 02114, USA.
A Sutton
N van Rooijen
J Stein-Streilein
Brigham and Women's Hospital · USMassachusetts Institute of Technology · USSmith-Kettlewell Eye Research Institute · USVrije Universiteit Amsterdam · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hapten immune pulmonary interstitial fibrosis (HIPIF) is induced by a recall cell-mediated immune response against the hapten 2,4, 6-trinitrobenzene sulphonic acid (TNBS) in the lung. Studies here dissect the role of the cellular components of the bronchoalveolar lavage (BAL) cells (alveolar macrophages [AMs] versus monocytes and immature dendritic cells) in the fibrogenic inflammatory response. BAL cells from HIPIF mice were generally more activated and produced a greater amount of tumour necrosis factor-alpha (TNF-alpha) than controls. Liposome-encapsulated dichloromethylene diphosphonate (Cl(2)MDP) that was inoculated intranasally (i.n.) into mice selectively depleted AMs. Following AM depletion, the number of TNF-alpha-containing cells was reduced, and both the number of immune inflammatory cells recruited into the alveolar space and the subsequent collagen deposition (hydroxyproline) were decreased in the sensitized and intratracheally (i.t.) challenged mice. In conclusion, AMs are required, in part, for the development of pulmonary fibrosis in HIPIF because AM-derived factors such as TNF-alpha are needed for initiation of chemokine and cytokine pathways and accumulation of immune inflammatory cells.

Indexed as

Adoptive TransferAnimalsAutoimmune DiseasesBronchoalveolar Lavage FluidDendritic CellsFemaleHaptensHydroxyprolineMacrophages, AlveolarMiceMice, Inbred BALB CMonocytesPulmonary FibrosisTrinitrobenzenesulfonic AcidTumor Necrosis Factor-alphaHaptensHydroxyprolineTrinitrobenzenesulfonic AcidTumor Necrosis Factor-alpha

Identifiers

PMID11122454
PMCPMC2327107
OpenAlexW1982916457

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.