Evidence map›Paper›PMID 29067996›Full record

ArticleMucosal immunology2018

The survival of fetal and bone marrow monocyte-derived alveolar macrophages is promoted by CD44 and its interaction with hyaluronan.

Y Dong, G F T Poon, A A Arif, S S M Lee-Sayer, M Dosanjh, P Johnson

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Mucosal immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Discovery of intrahepatic CD103Experimental & molecular medicine · 2025
    Article
  4. CD44 in Group 1 Innate Lymphoid Cells Impacts the Development and Progression of Steatohepatitis.Liver international : official journal of the International Association for the Study of the Liver · 2025
    Article
  5. Review
  6. Mast cells are key mediators in the pulmonary inflammatory response to formaldehyde exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2025
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. RepurposingViruses · 2023
    Article
  12. Review
  13. The role of lung macrophages in acute respiratory distress syndrome.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. On Top of the Alveolar Epithelium: Surfactant and the Glycocalyx.International journal of molecular sciences · 2020
    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

6 authors at 1 institution in 1 country.

Y DongDepartment of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia, Canada.
G F T PoonDepartment of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia, Canada.
A A ArifDepartment of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia, Canada.
S S M Lee-SayerDepartment of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia, Canada.
M DosanjhDepartment of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia, Canada.
P JohnsonDepartment of Microbiology and Immunology, University of British Columbia, Vancouver, British Columbia, Canada.
University of British Columbia · CA

Funding

CIHR MOP 119503
6 · The paper itself

Abstract

Alveolar macrophages maintain lung homeostasis by performing important roles in immunosurveillance and lung surfactant catabolism. They express high levels of CD44 and are one of the few macrophage populations that constitutively bind hyaluronan, a ligand for CD44 and component of pericellular and extracellular matrices. Using adoptive transfer experiments and a mouse model of inflammation, we found that alveolar macrophages are initially depleted after an inflammatory insult then rapidly self-renew and return to original numbers after the resolution phase. Monocytes recruited to an inflamed lung differentiate and contribute to the alveolar macrophage pool, but this occurs over a much slower time frame than alveolar macrophage self-renewal. CD44 expression on both fetal and bone marrow-derived alveolar macrophages promoted their survival and provided a competitive advantage over CD44-deficient alveolar macrophages at homeostasis and after inflammation. CD44-mediated hyaluronan binding was induced by the alveolar environment, and this interaction promoted alveolar macrophage survival both ex vivo and in vivo. Without CD44, alveolar macrophages lacked a hyaluronan coat, were more susceptible to death, and were present at lower numbers in the alveolar space. This demonstrates a new role for CD44 and hyaluronan in promoting alveolar macrophage survival.

Indexed as

AnimalsBone MarrowCell DifferentiationCells, CulturedCell SurvivalExtracellular MatrixFetusHomeostasisHyaluronan ReceptorsHyaluronic AcidLungMacrophages, AlveolarMiceMice, Inbred C57BLMice, KnockoutMonocytesHyaluronan ReceptorsHyaluronic Acid

Identifiers

PMID29067996
OpenAlexW2766532941

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.