Evidence map›Paper›PMID 24867320›Full record

ArticlePloS one2014

A novel antifungal is active against Candida albicans biofilms and inhibits mutagenic acetaldehyde production in vitro.

Mikko T Nieminen, Lily Novak-Frazer, Vilma Rautemaa, Ranjith Rajendran, Timo Sorsa, Gordon Ramage, Paul Bowyer, Riina Rautemaa

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
2.7field-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

20 citing papers in PubMed, 46 citations in OpenAlex.

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  13. Intestinal Infection ofFrontiers in microbiology · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 5 institutions in 2 countries.

Mikko T NieminenResearch Unit on Acetaldehyde and Cancer, University of Helsinki, Helsinki, Finland; Department of Periodontology, Institute of Dentistry, University of Helsinki, Helsinki, Finland; Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Helsinki, Finland; The University of Manchester, Institute of Inflammation and Repair, Manchester Academic Health Science Centre, University Hospital of South Manchester, Wythenshawe Hospital, Manchester, United Kingdom.
Lily Novak-FrazerThe University of Manchester, Institute of Inflammation and Repair, Manchester Academic Health Science Centre, University Hospital of South Manchester, Wythenshawe Hospital, Manchester, United Kingdom.
Vilma RautemaaThe University of Manchester, Institute of Inflammation and Repair, Manchester Academic Health Science Centre, University Hospital of South Manchester, Wythenshawe Hospital, Manchester, United Kingdom.
Ranjith RajendranInfection and Immunity Research Group, Glasgow Dental School and Hospital, School of Medicine, College of Medicine, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
Timo SorsaDepartment of Periodontology, Institute of Dentistry, University of Helsinki, Helsinki, Finland; Department of Oral and Maxillofacial Diseases, Helsinki University Central Hospital Finland, Helsinki, Finland.
Gordon RamageInfection and Immunity Research Group, Glasgow Dental School and Hospital, School of Medicine, College of Medicine, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom.
Paul BowyerThe University of Manchester, Institute of Inflammation and Repair, Manchester Academic Health Science Centre, University Hospital of South Manchester, Wythenshawe Hospital, Manchester, United Kingdom.
Riina RautemaaResearch Unit on Acetaldehyde and Cancer, University of Helsinki, Helsinki, Finland; Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Helsinki, Finland; Department of Oral and Maxillofacial Diseases, Helsinki University Central Hospital Finland, Helsinki, Finland; The University of Manchester, Institute of Inflammation and Repair, Manchester Academic Health Science Centre, University Hospital of South Manchester, Wythenshawe Hospital, Manchester, United Kingdom.
Manchester Academic Health Science Centre · GBUniversity of Glasgow · GBUniversity of Manchester · GBHelsinki University Hospital · FIWythenshawe Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The ability of C. albicans to form biofilms is a major virulence factor and a challenge for management. This is evident in biofilm-associated chronic oral-oesophageal candidosis, which has been shown to be potentially carcinogenic in vivo. We have previously shown that most Candida spp. can produce significant levels of mutagenic acetaldehyde (ACH). ACH is also an important mediator of candidal biofilm formation. We have also reported that D,L-2-hydroxyisocaproic acid (HICA) significantly inhibits planktonic growth of C. albicans. The aim of the present study was to investigate the effect of HICA on C. albicans biofilm formation and ACH production in vitro. Inhibition of biofilm formation by HICA, analogous control compounds or caspofungin was measured using XTT to measure biofilm metabolic activity and PicoGreen as a marker of biomass. Biofilms were visualised by scanning electron microscopy (SEM). ACH levels were measured by gas chromatography. Transcriptional changes in the genes involved in ACH metabolism were measured using RT-qPCR. The mean metabolic activity and biomass of all pre-grown (4, 24, 48 h) biofilms were significantly reduced after exposure to HICA (p<0.05) with the largest reductions seen at acidic pH. Caspofungin was mainly active against biofilms pre-grown for 4 h at neutral pH. Mutagenic levels (>40 µM) of ACH were detected in 24 and 48 h biofilms at both pHs. Interestingly, no ACH production was detected from D-glucose in the presence of HICA at acidic pH (p<0.05). Expression of genes responsible for ACH catabolism was up-regulated by HICA but down-regulated by caspofungin. SEM showed aberrant hyphae and collapsed hyphal structures during incubation with HICA at acidic pH. We conclude that HICA has potential as an antifungal agent with ability to inhibit C. albicans cell growth and biofilm formation. HICA also significantly reduces the mutagenic potential of C. albicans biofilms, which may be important when treating bacterial-fungal biofilm infections.

Indexed as

AcetaldehydeAntifungal AgentsBiofilmsCandida albicansCandidiasisCaproatesCell ProliferationIn Vitro TechniquesMicrobial Sensitivity TestsMicroscopy, Electron, ScanningMutagensReal-Time Polymerase Chain ReactionAcetaldehydealpha-hydroxyisocaproic acidAntifungal AgentsCaproatesMutagens

Identifiers

PMID24867320
PMCPMC4035295
OpenAlexW2025270703

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.