Evidence map›Paper›PMID 25394861›Full record

ReviewSeminars in immunopathology2015

Candida albicans phospholipomannan: a sweet spot for controlling host response/inflammation.

Chantal Fradin, Emerson Soares Bernardes, Thierry Jouault

Abstract readReview
PubMed Publisher
In one paragraph

Review in Seminars in immunopathology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

8 citing papers in PubMed, 14 citations in OpenAlex.

  1. Review
  2. Article
  3. On Commensalism ofJournal of fungi (Basel, Switzerland) · 2020
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. 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

3 authors at 2 institutions in 2 countries.

Chantal FradinInserm U995, 59000, Lille, France.
Emerson Soares Bernardes
Thierry Jouault
Inserm · FRNational Nuclear Energy Commission · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fungal cell walls contain several types of glycans, which play important roles in the pathogenesis of fungal infection and host immune response. Among them, glycosphingolipids have attracted much attention lately since they contribute actively to the fungi development and fungal-induced pathogenesis. Although glycosphingolipids are present in pathogenic and non-pathogenic fungi, pathogenic strains exhibit distinct glycan structures on their sphingolipids, which contribute to the regulatory processes engaged in inflammatory response. In Candida albicans, phospholipomannan (PLM) represents a prototype of these sphingolipids. Through its glycan and lipid moieties, PLM induces activation of host signaling pathways involved in the initial recognition of fungi, causing immune system disorder and persistent fungal disease. In this review, first we describe the general aspects of C. albicans sphingolipids synthesis with a special emphasize on PLM synthesis and its insertion into the cell wall. Then, we discuss the role of PLM glycosylation in regulating immune system activation and its contribution to the chronic persistent inflammation found in Candida infections and chronic inflammatory diseases.

Indexed as

Candida albicansCandidiasisGlycolipidsGlycosphingolipidsHost-Pathogen InteractionsHumansImmunomodulationMacrophage ActivationMacrophagesPolysaccharidesReceptors, Pattern RecognitionSignal TransductionSphingolipidsGlycolipidsGlycosphingolipidsphospholipomannanPolysaccharidesReceptors, Pattern RecognitionSphingolipids

Identifiers

PMID25394861
OpenAlexW2140244176

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.