Evidence map›Paper›PMID 19609651›Full record

ArticleMolecular and cellular biochemistry2010

Role of phosphatidylinositol-3-kinase (PI3K), extracellular signal-regulated kinase (ERK) and nuclear transcription factor kappa beta (NF-k beta) on neutrophil phagocytic process of Candida albicans.

E Giraldo, L Martin-Cordero, M D Hinchado, J J Garcia, E Ortega

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.0field-weighted citation impact, top 27% 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

9 citing papers in PubMed, 18 citations in OpenAlex.

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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 1 institution in 1 country.

E GiraldoDepartment of Physiology, Faculty of Sciences, University of Extremadura, 06071, Badajoz, Spain.
L Martin-Cordero
M D Hinchado
J J Garcia
E Ortega
Universidad de Extremadura · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In humans, Candida albicans is the microorganism most frequently associated with fungal infections. Alterations in the balance between the host and this commensal pathogen, turns into a parasitic relationship which results in the development of invasive infections. Neutrophils via chemotaxis, phagocytosis, and microbicide capacity can eradicate this pathogen. Taken together, the aim of this work was to study the possible role of phosphatidylinositol-3-kinase (PI3K), extracellular signal-regulated kinase (ERK) and the nuclear transcription factor kappa beta (NF-k beta) on the phagocytic process of neutrophils. The chemotactic capacity of neutrophils and their ability to phagocytose and to destroy C. albicans in absence and presence of 1, 10, or 100 microM of wortmannin (a PI3K inhibitor); 10, 25, or 50 microM of Bay 11-7082 (a NF-k beta inhibitor) or 1, 5 or 10 microM of PD 98,059 (an ERK inhibitor) were determined. Our results show that fMLP-induced chemotaxis needs the participation of PI3K and NF-k beta. In contrast, ERK seems not to be involved. On the other hand, the inhibition of NF-kappa beta and ERK decreased neutrophil phagocytosis and microbicide capacity against C. albicans. However, both the phagocytic and candicide capacities were PI3K independent.

Indexed as

PhagocytosisAdultCandida albicansCells, CulturedChemotaxisEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesFemaleHumansNeutrophilsNF-kappa BPhosphatidylinositol 3-KinasesYoung AdultEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesNF-kappa BPhosphatidylinositol 3-Kinases

Identifiers

PMID19609651
OpenAlexW2035815938

What Socratic 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 Socratic graph.