Evidence map›Paper›PMID 25916991›Full record

ArticleInfection and immunity2015

Evidence for Proinflammatory β-1,6 Glucans in the Pneumocystis carinii Cell Wall.

Theodore J Kottom, Deanne M Hebrink, Paige E Jenson, Gunnar Gudmundsson, Andrew H Limper

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Antioxidants (Basel, Switzerland) · 2026
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  7. Metabolic modulation:Cell surface (Amsterdam, Netherlands) · 2024
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  8. Characterization of theAntimicrobial agents and chemotherapy · 2024
    Article
  9. Article
  10. Article
  11. Targeting β-glucans, vital components of theFrontiers in immunology · 2023
    Review
  12. Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. The Contribution of Host Cells toPathogens (Basel, Switzerland) · 2019
    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

5 authors at 2 institutions in 2 countries.

Theodore J KottomThoracic Diseases Research Unit, Departments of Medicine and Biochemistry, Mayo Clinic College of Medicine, Rochester, Minnesota, USA University of Iceland School of Health Sciences, Reykjavík, Iceland.
Deanne M HebrinkThoracic Diseases Research Unit, Departments of Medicine and Biochemistry, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Paige E JensonThoracic Diseases Research Unit, Departments of Medicine and Biochemistry, Mayo Clinic College of Medicine, Rochester, Minnesota, USA.
Gunnar GudmundssonUniversity of Iceland School of Health Sciences, Reykjavík, Iceland.
Andrew H LimperThoracic Diseases Research Unit, Departments of Medicine and Biochemistry, Mayo Clinic College of Medicine, Rochester, Minnesota, USA limper.andrew@mayo.edu.
Mayo Clinic · USUniversity of Iceland · IS

Funding

Pneumocystis: Macrophage & Epithelial ActivationR01HL062150 · NHLBI · MAYO CLINIC ROCHESTER · PI ANDREW H LIMPER · 1998 to 2026
$9.2M
NHLBI NIH HHS R01 HL062150NHLBI NIH HHS R01-HL62150
6 · The paper itself

Abstract

Inflammation is a major cause of respiratory impairment during Pneumocystis pneumonia. Studies support a significant role for cell wall β-glucans in stimulating inflammatory responses. Fungal β-glucans are comprised of d-glucose homopolymers containing β-1,3-linked glucose backbones with β-1,6-linked glucose side chains. Prior studies in Pneumocystis carinii have characterized β-1,3 glucan components of the organism. However, recent investigations in other organisms support important roles for β-1,6 glucans, predominantly in mediating host cellular activation. Accordingly, we sought to characterize β-1,6 glucans in the cell wall of Pneumocystis and to establish their activity in lung cell inflammation. Immune staining revealed specific β-1,6 localization in P. carinii cyst walls. Homology-based cloning facilitated characterization of a functional P. carinii kre6 (Pckre6) β-1,6 glucan synthase in Pneumocystis that, when expressed in kre6-deficient Saccharomyces cerevisiae, restored cell wall stability. Recently synthesized β-1,6 glucan synthase inhibitors decreased the ability of isolated P. carinii preparations to generate β-1,6 carbohydrate. In addition, isolated β-1,6 glucan fractions from Pneumocystis elicited vigorous tumor necrosis factor alpha (TNF-α) responses from macrophages. These inflammatory responses were significantly dampened by inhibition of host cell plasma membrane microdomain function. Together, these studies indicate that β-1,6 glucans are present in the P. carinii cell wall and contribute to lung cell inflammatory activation during infection.

Indexed as

Animalsbeta-GlucansCell LineCell WallCloning, MolecularGlucosyltransferasesMacrophagesMicePneumocystis cariniiSaccharomyces cerevisiaebeta-GlucansGlucosyltransferases

Identifiers

PMID25916991
PMCPMC4468544
OpenAlexW2285228239

What OpenQuestion holds

Textmetadata
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Registered trials

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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.