Evidence map›Paper›PMID 32363390›Full record

ArticleThe Journal of infectious diseases2020

Pneumocystis carinii Major Surface Glycoprotein Dampens Macrophage Inflammatory Responses to Fungal β-Glucan.

Theodore J Kottom, Deanne M Hebrink, Eva M Carmona, Andrew H Limper

Open access · greenAbstract read
In one paragraph

Article in The Journal of infectious diseases, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

10 citing papers in PubMed, 10 citations in OpenAlex.

  1. Strain-Dependent Protective Innate Immunity AgainstJournal of fungi (Basel, Switzerland) · 2026
    Article
  2. Review
  3. Infection and immunity · 2026
    Article
  4. Article
  5. Article
  6. Retracing the evolution ofMicrobiology and molecular biology reviews : MMBR · 2024
    Review
  7. Article
  8. Targeting β-glucans, vital components of theFrontiers in immunology · 2023
    Review
  9. Article
  10. 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.

Theodore J KottomThoracic Diseases Research Unit, Departments of Medicine and Biochemistry, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Deanne M HebrinkThoracic Diseases Research Unit, Departments of Medicine and Biochemistry, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Eva M CarmonaThoracic Diseases Research Unit, Departments of Medicine and Biochemistry, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Andrew H LimperThoracic Diseases Research Unit, Departments of Medicine and Biochemistry, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Mayo Clinic · US

Funding

Pneumocystis: Macrophage & Epithelial ActivationR01HL062150 · NHLBI · MAYO CLINIC ROCHESTER · PI ANDREW H LIMPER · 1998 to 2026
$9.2M
NHLBI NIH HHS R01 HL062150
6 · The paper itself

Abstract

backgroundPneumocystis major surface glycoprotein (Msg) is a 120-kD surface protein complex on the organism with importance in adhesion and immune recognition. In this study, we show that Msg significantly impairs tumor necrosis factor (TNF)-α secretion by macrophages induced by Saccharomyces cerevisiae and Pneumocystis carinii (Pc) β-glucans.

methodsMajor surface glycoprotein was shown to greatly reduce β-glucan-induced Dectin-1 immunoreceptor tyrosine-based activating motif (ITAM) phosphorylation. Major surface glycoprotein also down regulated Dectin-1 receptor messenger ribonucleic acid (mRNA) expression in the macrophages. It is interesting that Msg incubation with macrophages resulted in significant mRNA upregulation of both C-type lectin receptors (CLR) Mincle and MCL in Msg protein presence alone but to even greater amounts in the presence of Pc β-glucan.

resultsThe silencing of MCL and Mincle resulted in TNF-α secretions similar to that of macrophages treated with Pneumocystis β-glucan alone, which is suggestive of an inhibitory role for these 2 CLRs in Msg-suppressive effects on host cell immune response.

conclusionsTaken together, these data indicate that the Pneumocystis Msg surface protein complex can act to suppress host macrophage inflammatory responses to the proinflammatory β -glucan components of the organisms.

Indexed as

Animalsbeta-GlucansFungal ProteinsLectins, C-TypeMacrophagesMembrane GlycoproteinsMicePneumocystisPneumocystis cariniiPneumonia, PneumocystisRAW 264.7 CellsRNA, MessengerSaccharomyces cerevisiaeTumor Necrosis Factor-alphabeta-GlucansFungal ProteinsLectins, C-TypeMembrane GlycoproteinsRNA, MessengerTumor Necrosis Factor-alphamajor surface glycoproteinMCLMincleMsgPneumocystis

Identifiers

PMID32363390
PMCPMC7459132
OpenAlexW3023586050

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.