Evidence map›Paper›PMID 26684322›Full record

ArticleParasites & vectors2015

Studies in the mouse model identify strain variability as a major determinant of disease outcome in Leishmania infantum infection.

Filipe Marques, Sílvia Vale-Costa, Tânia Cruz, Joana Moreira Marques, Tânia Silva, João Vilares Neves, Sofia Cortes, Ana Fernandes, Eduardo Rocha, Rui Appelberg and 3 more

Open access · goldAbstract read
In one paragraph

Article in Parasites & vectors, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.7field-weighted citation impact, top 23% 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

4 citing papers in PubMed, 10 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

13 authors at 3 institutions in 3 countries.

Filipe MarquesInstituto de Investigação e Inovação em Saúde and IBMC, Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal. Filipe.Marques@ibmc.up.pt.
Sílvia Vale-CostaInstituto de Investigação e Inovação em Saúde and IBMC, Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal. svcosta@igc.gulbenkian.pt.
Tânia CruzInstituto de Investigação e Inovação em Saúde and IBMC, Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal. TCruz@ibmc.up.pt.
Joana Moreira MarquesInstituto de Investigação e Inovação em Saúde and IBMC, Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal. joana.amc.marques@gmail.com.
Tânia SilvaInstituto de Investigação e Inovação em Saúde; IBMC, Instituto de Biologia Molecular e Celular, and ICBAS, Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, Porto, Portugal. Tania.Silva@ibmc.up.pt.
João Vilares NevesInstituto de Investigação e Inovação em Saúde and IBMC, Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal. JNeves@ibmc.up.pt.
Sofia CortesGHTM, Global Health and Tropical Medicine, IHMT, Instituto de Higiene e Medicina Tropical, Universidade Nova de Lisboa, Lisbon, Portugal. SCortes@ihmt.unl.pt.
Ana FernandesICBAS, Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, Porto, Portugal. anaisabelmfernandes@gmail.com.
Eduardo RochaICBAS, Instituto de Ciências Biomédicas Abel Salazar, and CIIMAR, Centro Interdisciplinar de Investigação Marinha e Ambiental, Universidade do Porto, Porto, Portugal. erocha@icbas.up.pt.
Rui AppelbergInstituto de Investigação e Inovação em Saúde; IBMC, Instituto de Biologia Molecular e Celular, and ICBAS, Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, Porto, Portugal. rappelb@ibmc.up.pt.
Pedro RodriguesInstituto de Investigação e Inovação em Saúde; IBMC, Instituto de Biologia Molecular e Celular, and ICBAS, Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, Porto, Portugal. prodrigu@ibmc.up.pt.
Ana M TomásInstituto de Investigação e Inovação em Saúde; IBMC, Instituto de Biologia Molecular e Celular, and ICBAS, Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, Porto, Portugal. atomas@ibmc.up.pt.
Maria Salomé GomesInstituto de Investigação e Inovação em Saúde; IBMC, Instituto de Biologia Molecular e Celular, and ICBAS, Instituto de Ciências Biomédicas Abel Salazar, Universidade do Porto, Porto, Portugal. sgomes@ibmc.up.pt.
Universidade do Porto · PTi3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto · PTTechnical University of Applied Sciences Wildau · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundVisceral leishmaniasis is a severe and potentially fatal disease caused by protozoa of the genus Leishmania, transmitted by phlebotomine sandflies. In Europe and the Mediterranean region, L. infantum is the commonest agent of visceral leishmaniasis, causing a wide spectrum of clinical manifestations, including asymptomatic carriage, cutaneous lesions and severe visceral disease. Visceral leishmaniasis is more frequent in immunocompromised individuals and data obtained in experimental models of infection have highlighted the importance of the host immune response, namely the efficient activation of host's macrophages, in determining infection outcome. Conversely, few studies have addressed a possible contribution of parasite variability to this outcome.

methodsIn this study, we compared three isolates of L. infantum regarding their capacity to grow in the organs of mice, the way they activate the host's macrophages and other components of the immune response and also their capacity to cope with host's antimicrobial mechanisms, namely reactive oxygen and nitrogen species.

resultsWe found that the three parasite strains significantly differed regarding the degree to which they induced nitric oxide synthase (NOS2) and arginase expression in infected macrophages and the pattern of cytokine production they induced in the host, resulting in different degrees of inflammatory response in infected livers. Additionally, the three strains also significantly differed in their in vitro susceptibility to reactive oxygen and nitrogen species. This variability was reflected in the capacity of each strain to persist and proliferate in the organs of wild-type as well as NOS2- and phagocyte oxidase- deficient mice.

conclusionsThe results obtained in this study show that parasite strain variability is an important determinant of disease outcome in L. infantum visceral leishmaniasis, with relevant implications for studies on host-pathogen interaction and also for leishmanicidal drug development.

Indexed as

Genetic VariationAnimalsAnimal StructuresDisease Models, AnimalHost-Pathogen InteractionsLeishmania infantumLeishmaniasis, VisceralMacrophage ActivationMiceReactive Nitrogen SpeciesReactive Oxygen SpeciesTreatment OutcomeVirulenceReactive Nitrogen SpeciesReactive Oxygen Species

Identifiers

PMID26684322
PMCPMC4684599
OpenAlexW2199808155

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.