Evidence map›Paper›PMID 24667630›Full record

ArticleShock (Augusta, Ga.)2014

Itraconazole, a commonly used antifungal, inhibits Fcγ receptor-mediated phagocytosis: alteration of Fcγ receptor glycosylation and gene expression.

Diego F Niño, David M Cauvi, Antonio De Maio

Open access · greenAbstract read
In one paragraph

Article in Shock (Augusta, Ga.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
3.0field-weighted citation impact, top 10% 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

6 citing papers in PubMed, 13 citations in OpenAlex.

  1. Article
  2. Small molecule-mediated inhibition of myofibroblast transdifferentiation for the treatment of fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  3. Article
  4. Article
  5. Article
  6. 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 1 institution in 1 country.

Diego F Niño*Biomedical Sciences Graduate Program,Departments of †Surgery and ‡Neurosciences and §The Center for Investigations of Health and Education Disparities, University of California, San Diego, La Jolla, California.
David M Cauvi
Antonio De Maio
Center for Neurosciences · US

Funding

Mentoring Young Minds to Increase Diversity in the Biomedical ResearchR25GM083275 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI DE MAIO, ANTONIO, LAWSON, MARK ANDREW · 2008 to 2022
$9.9M
CD14: Biosynthesis, Trafficking and SecretionF31GM090681 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI NINO, DIEGO FERNANDO · 2010 to 2013
$126k
NIGMS NIH HHS F31 GM090681NIGMS NIH HHS R01 GM083275NIGMS NIH HHS R25 GM083275
6 · The paper itself

Abstract

Itraconazole (ICZ) is commonly used for the treatment of fungal infections, particularly in immunocompromised patients. In addition, ICZ has been recently found to have antiangiogenic effects and is currently being tested as a new chemotherapeutic agent in several cancer clinical trials. We have previously shown that ICZ impaired complex N-linked glycosylation processing, leading to the accumulation of high-mannose glycoproteins on the surface of macrophages (Møs). This investigation was directed at determining the effects of ICZ on phagocytosis as a major function of Møs. We found a significant decrease in the phagocytosis of opsonized bacterial particles in ICZ-treated murine Møs in comparison with nontreated Møs. Furthermore, the impairment of phagocytosis was associated with a decrease in cell surface expression of Fcγ receptors (FcγRs) as well as alteration of their glycosylation pattern. Concomitantly, a reduction in all three isoforms of the FcγR family (i.e., Fcgr1, Fcgr2, and Fcgr3) mRNA levels was observed after incubation with ICZ. The effect of ICZ on phagocytosis and FcγR expression was reversed by addition of low-density lipoprotein. These studies indicate that ICZ treatment certainly has a dramatic effect on macrophage function, which could result in a potential impairment of the immune system';s ability to respond to pathogens and may lead to an elevated incidence of infections.

Indexed as

AnimalsAntifungal AgentsCell MembraneCells, CulturedCholesterol, LDLDose-Response Relationship, DrugEscherichia coliGene Expression RegulationGlycosylationItraconazoleMacrophagesMaleMice, Inbred StrainsPhagocytosisReceptors, IgGAntifungal AgentsCholesterol, LDLItraconazoleReceptors, IgG

Identifiers

PMID24667630
PMCPMC4071940
OpenAlexW2084505631

What OpenQuestion holds

Textmetadata
LicenceTDM
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.