Evidence map›Paper›PMID 23408887›Full record

ArticlePLoS pathogens2013

Plasmodium falciparum malaria elicits inflammatory responses that dysregulate placental amino acid transport.

Philippe Boeuf, Elizabeth H Aitken, Upeksha Chandrasiri, Caroline Lin Lin Chua, Bernie McInerney, Leon McQuade, Michael Duffy, Malcolm Molyneux, Graham Brown, Jocelyn Glazier and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

42 citing papers in PubMed, 83 citations in OpenAlex.

  1. Trial
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  3. Co-infection ofIJID regions · 2024
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  5. Homeostasis Maintenance inFrontiers in immunology · 2022
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  6. Article
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  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. An overview of malaria in pregnancy.Seminars in perinatology · 2019
    Review
  16. Establishing a conceptual framework of the impact of placental malaria on infant neurodevelopment.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2019
    Review
  17. Article
  18. Article
  19. Article
  20. 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

11 authors at 5 institutions in 3 countries.

Philippe BoeufThe University of Melbourne, Department of Medicine-RMH, Parkville, Victoria, Australia. pboeuf@unimelb.edu.au
Elizabeth H Aitken
Upeksha Chandrasiri
Caroline Lin Lin Chua
Bernie McInerney
Leon McQuade
Michael Duffy
Malcolm Molyneux
Graham Brown
Jocelyn Glazier
Stephen J Rogerson
University of Melbourne · AUMacquarie University · AUMalawi-Liverpool-Wellcome Trust Clinical Research Programme · MWSt Mary's Hospital · GBThe Royal Melbourne Hospital · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Placental malaria (PM) can lead to poor neonatal outcomes, including low birthweight due to fetal growth restriction (FGR), especially when associated with local inflammation (intervillositis or IV). The pathogenesis of PM-associated FGR is largely unknown, but in idiopathic FGR, impaired transplacental amino acid transport, especially through the system A group of amino acid transporters, has been implicated. We hypothesized that PM-associated FGR could result from impairment of transplacental amino acid transport triggered by IV. In a cohort of Malawian women and their infants, the expression and activity of system A (measured by Na⁺-dependent ¹⁴C-MeAIB uptake) were reduced in PM, especially when associated with IV, compared to uninfected placentas. In an in vitro model of PM with IV, placental cells exposed to monocyte/infected erythrocytes conditioned medium showed decreased system A activity. Amino acid concentrations analyzed by reversed phase ultra performance liquid chromatography in paired maternal and cord plasmas revealed specific alterations of amino acid transport by PM, especially with IV. Overall, our data suggest that the fetoplacental unit responds to PM by altering its placental amino acid transport to maintain adequate fetal growth. However, IV more profoundly compromises placental amino acid transport function, leading to FGR. Our study offers the first pathogenetic explanation for FGR in PM.

Indexed as

AdolescentAdultAmino AcidsAmino Acid Transport System ABiological TransportCase-Control StudiesCell Line, TumorCohort StudiesFemaleFetal Growth RetardationHumansInfantInfant, Low Birth WeightInfant, NewbornInterleukin-1betaMalaria, FalciparumAmino AcidsAmino Acid Transport System AInterleukin-1betaSLC38A1 protein, humanSLC38A2 protein, human

Identifiers

PMID23408887
PMCPMC3567154
OpenAlexW2029155139

What OpenQuestion holds

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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.