Evidence map›Paper›PMID 14573639›Full record

ArticleInfection and immunity2003

Absence of the macrophage mannose receptor in mice does not increase susceptibility to Pneumocystis carinii infection in vivo.

Steve D Swain, Sena J Lee, Michel C Nussenzweig, Allen G Harmsen

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

51 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
  2. Article
  3. Immunity to fungi in the lung.Seminars in immunology · 2023
    Review
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  7. Review
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  9. Article
  10. Quantitative Analysis of Polysaccharide Composition inMolecules (Basel, Switzerland) · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Fungal Strategies to Evade the Host Immune Recognition.Journal of fungi (Basel, Switzerland) · 2017
    Review
  16. Article
  17. Article
  18. Article
  19. 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 2 institutions in 1 country.

Steve D SwainDepartment of Veterinary Molecular Biology, Montana State University, Bozeman, Montana 59717, USA. uvsss@montana.edu
Sena J Lee
Michel C Nussenzweig
Allen G Harmsen
Montana State University · USRockefeller University · US

Funding

PROJECT4--- THE INFLAMMATORY RESPONSE: IMPACT ON THE OUTCOME OF PCPP01HL071659 · NHLBI · UNIVERSITY OF ROCHESTER · PI GIGLIOTTI, FRANCIS · 2002 to 2006
$7.4M
RECONSTITUTION OF IMMUNITY TO PNEUMOCYSTIS IN SCID MICER01HL055002 · NHLBI · TRUDEAU INSTITUTE, INC. · PI HARMSEN, ALLEN G · 1995 to 2009
$3.5M
NHLBI NIH HHS HL55002NHLBI NIH HHS HL71659NHLBI NIH HHS P01 HL071659NHLBI NIH HHS R01 HL055002
6 · The paper itself

Abstract

Host defense against the opportunistic pathogen Pneumocystis carinii requires functional interactions of many cell types. Alveolar macrophages are presumed to be a vital host cell in the clearance of P. carinii, and the mechanisms of this interaction have come under scrutiny. The macrophage mannose receptor is believed to play an important role as a receptor involved in the binding and phagocytosis of P. carinii. Although there is in vitro evidence for this interaction, the in vivo role of this receptor in P. carinii clearance in unclear. Using a mouse model in which the mannose receptor has been deleted, we found that the absence of this receptor is not sufficient to allow infection by P. carinii in otherwise immunocompetent mice. Furthermore, when mice were rendered susceptible to P. carinii by CD4(+) depletion, mannose receptor knockout mice (MR-KO) had pathogen loads equal to those of wild-type mice. However, the MR-KO mice exhibited a greater influx of phagocytes into the alveoli during infection. This was accompanied by increased pulmonary pathology in the MR-KO mice, as well as greater accumulation of glycoproteins in the alveoli (glycoproteins, including harmful hydrolytic enzymes, are normally cleared by the mannose receptor). We also found that the surface expression of the mannose receptor is not downregulated during P. carinii infection in wild-type mice. Our findings suggest that while the macrophage mannose receptor may be important in the recognition of P. carinii, in vivo, this mechanism may be redundant, and the absence of this receptor may be compensated for.

Indexed as

AnimalsCD4-Positive T-LymphocytesDisease SusceptibilityLectins, C-TypeMacrophagesMannoseMannose-Binding LectinsMannose ReceptorMiceMice, Inbred C57BLMice, KnockoutPneumocystis InfectionsReceptors, Cell SurfaceSerum Albumin, BovineLectins, C-TypeMannoseMannose-Binding LectinsMannose ReceptorReceptors, Cell SurfaceSerum Albumin, Bovine

Identifiers

PMID14573639
PMCPMC219593
OpenAlexW2124077127

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.