Evidence map›Paper›PMID 29506544›Full record

ArticleMalaria journal2018

Experimental malaria-associated acute respiratory distress syndrome is dependent on the parasite-host combination and coincides with normocyte invasion.

Leen Vandermosten, Thao-Thy Pham, Hendrik Possemiers, Sofie Knoops, Evelien Van Herck, Julie Deckers, Blandine Franke-Fayard, Tracey J Lamb, Chris J Janse, Ghislain Opdenakker and 1 more

Open access · goldAbstract read
In one paragraph

Article in Malaria journal, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.2field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  15. Pharmaceuticals (Basel, Switzerland) · 2023
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  18. Review
  19. Brain endothelial STING1 activation byProceedings of the National Academy of Sciences of the United States of America · 2022
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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

11 authors at 4 institutions in 3 countries.

Leen VandermostenLaboratory of Immunobiology, Department of Microbiology and Immunology, Rega Institute for Medical Research, KU Leuven-University of Leuven, Herestraat 49, box 1044, 3000, Leuven, Belgium.
Thao-Thy PhamLaboratory of Immunobiology, Department of Microbiology and Immunology, Rega Institute for Medical Research, KU Leuven-University of Leuven, Herestraat 49, box 1044, 3000, Leuven, Belgium.
Hendrik PossemiersLaboratory of Immunobiology, Department of Microbiology and Immunology, Rega Institute for Medical Research, KU Leuven-University of Leuven, Herestraat 49, box 1044, 3000, Leuven, Belgium.
Sofie KnoopsLaboratory of Immunobiology, Department of Microbiology and Immunology, Rega Institute for Medical Research, KU Leuven-University of Leuven, Herestraat 49, box 1044, 3000, Leuven, Belgium.
Evelien Van HerckLaboratory of Immunobiology, Department of Microbiology and Immunology, Rega Institute for Medical Research, KU Leuven-University of Leuven, Herestraat 49, box 1044, 3000, Leuven, Belgium.
Julie DeckersLaboratory of Immunobiology, Department of Microbiology and Immunology, Rega Institute for Medical Research, KU Leuven-University of Leuven, Herestraat 49, box 1044, 3000, Leuven, Belgium.
Blandine Franke-FayardLeiden Malaria Research Group, Department of Parasitology, Leiden University Medical Center (LUMC), Albinusdreef 2, 2333 ZA, Leiden, The Netherlands.
Tracey J LambDepartment of Pathology, University of Utah, 15 N Medical Drive E, Salt Lake City, UT, 84112, USA.
Chris J JanseLeiden Malaria Research Group, Department of Parasitology, Leiden University Medical Center (LUMC), Albinusdreef 2, 2333 ZA, Leiden, The Netherlands.
Ghislain OpdenakkerLaboratory of Immunobiology, Department of Microbiology and Immunology, Rega Institute for Medical Research, KU Leuven-University of Leuven, Herestraat 49, box 1044, 3000, Leuven, Belgium.
Philippe E Van den SteenLaboratory of Immunobiology, Department of Microbiology and Immunology, Rega Institute for Medical Research, KU Leuven-University of Leuven, Herestraat 49, box 1044, 3000, Leuven, Belgium. philippe.vandensteen@kuleuven.be.
KU Leuven · BERega Institute for Medical Research · BELeiden University Medical Center · NLUniversity of Utah · US

Funding

Research Fund of the KU Leuven C1 project C16/17/010Research Fund of the KU Leuven GOA 2013/014
6 · The paper itself

Abstract

backgroundMalaria-associated acute respiratory distress syndrome (MA-ARDS) is a complication of malaria with a lethality rate of up to 80% despite anti-malarial treatment. It is characterized by a vast infiltration of leukocytes, microhaemorrhages and vasogenic oedema in the lungs. Previously, a mouse model for MA-ARDS was developed by infection of C57BL/6 mice with the Edinburgh line NK65-E of Plasmodium berghei.

resultsHere, both host and parasite factors were demonstrated to play crucial roles in the development and severity of lung pathology. In particular, the genetic constitution of the host was an important determinant in the development of MA-ARDS. Both male and female C57BL/6, but not BALB/c, mice developed MA-ARDS when infected with P. berghei NK65-E. However, the New York line of P. berghei NK65 (NK65-NY) did not induce demonstrable MA-ARDS, despite its accumulation in the lungs and fat tissue to a similar or even higher extent as P. berghei NK65-E. These two commonly used lines of P. berghei differ in their red blood cell preference. P. berghei NK65-NY showed a stronger predilection for reticulocytes than P. berghei NK65-E and this appeared to be associated with a lower pathogenicity in the lungs. The pulmonary pathology in the C57BL/6/P. berghei NK65-E model was more pronounced than in the model with infection of DBA/2 mice with P. berghei strain ANKA. The transient lung pathology in DBA/2 mice infected with P. berghei ANKA coincided with the infection phase in which parasites mainly infected normocytes. This phase was followed by a less pathogenic phase in which P. berghei ANKA mainly infected reticulocytes.

conclusionsThe propensity of mice to develop MA-ARDS during P. berghei infection depends on both host and parasite factors and appears to correlate with RBC preference. These data provide insights in induction of MA-ARDS and may guide the choice of different mouse-parasite combinations to study lung pathology.

Indexed as

Disease Models, AnimalAnimalsFemaleHost-Parasite InteractionsLungMalariaMaleMice, Inbred BALB CMice, Inbred C57BLPlasmodium bergheiRespiratory Distress SyndromeLungMalaria-associated acute respiratory distress syndromeNormocytePlasmodium bergheiReticulocyte

Identifiers

PMID29506544
PMCPMC5839036
OpenAlexW2798255562

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.