Evidence map›Paper›PMID 38711063›Full record

ArticleParasites & vectors2024

Contribution of parasite and host genotype to immunopathology of schistosome infections.

Kathrin S Jutzeler, Winka Le Clec'h, Frédéric D Chevalier, Timothy J C Anderson

Abstract read
In one paragraph

Article in Parasites & vectors, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

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  8. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors.

Kathrin S JutzelerHost Parasite Interaction Program, Texas Biomedical Research Institute, P.O. Box 760549, San Antonio, TX, 78245, USA. kjutzeler@txbiomed.org.ORCID http://orcid.org/0000-0002-3687-4020
Winka Le Clec'hHost Parasite Interaction Program, Texas Biomedical Research Institute, P.O. Box 760549, San Antonio, TX, 78245, USA.ORCID http://orcid.org/0000-0002-1111-2492
Frédéric D ChevalierHost Parasite Interaction Program, Texas Biomedical Research Institute, P.O. Box 760549, San Antonio, TX, 78245, USA.ORCID http://orcid.org/0000-0003-2611-8106
Timothy J C AndersonDisease Intervention and Prevention Program, Texas Biomedical Research Institute, P.O. Box 760549, San Antonio, TX, 78245, USA. tanderso@txbiomed.org.ORCID http://orcid.org/0000-0002-0191-0204

Funding

Genomic consequences of schistosome hybridizationR01AI166049 · NIAID · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI ANDERSON, TIM J · 2021 to 2025
$3.1M
Genetic analysis of cercarial release in schistosomesR01AI133749 · NIAID · TEXAS BIOMEDICAL RESEARCH INSTITUTE · PI ANDERSON, TIM J · 2017 to 2021
$2.5M
Graduate Research in Immunology Program (GRIP): To train graduate students for successful careers in academia, industry and governmentT32AI138944 · NIAID · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI ZHONG, GUANGMING · 2018 to 2022
$561k
NIAID NIH HHS R01 AI133749NIAID NIH HHS R01 AI166049NIAID NIH HHS T32 AI138944NIH HHS R01AI133749NIH HHS T32AI138944
6 · The paper itself

Abstract

backgroundThe role of pathogen genotype in determining disease severity and immunopathology has been studied intensively in microbial pathogens including bacteria, fungi, protozoa and viruses but is poorly understood in parasitic helminths. The medically important blood fluke Schistosoma mansoni is an excellent model system to study the impact of helminth genetic variation on immunopathology. Our laboratory has demonstrated that laboratory schistosome populations differ in sporocyst growth and cercarial production in the intermediate snail host and worm establishment and fecundity in the vertebrate host. Here, we (i) investigate the hypothesis that schistosome genotype plays a significant role in immunopathology and related parasite life history traits in the vertebrate mouse host and (ii) quantify the relative impact of parasite and host genetics on infection outcomes.

methodsWe infected BALB/c and C57BL/6 mice with four different laboratory schistosome populations from Africa and the Americas. We quantified disease progression in the vertebrate host by measuring body weight and complete blood count (CBC) with differential over a 12-week infection period. On sacrifice, we assessed parasitological (egg and worm counts, fecundity), immunopathological (organ measurements and histopathology) and immunological (CBC with differential and cytokine profiles) characteristics to determine the impact of parasite and host genetics.

resultsWe found significant variation between parasite populations in worm numbers, fecundity, liver and intestine egg counts, liver and spleen weight, and fibrotic area but not in granuloma size. Variation in organ weight was explained by egg burden and intrinsic parasite factors independent of egg burden. We found significant variation between infected mouse lines in cytokine levels (IFN-γ, TNF-α), eosinophils, lymphocytes and monocyte counts.

conclusionsThis study showed that both parasite and host genotype impact the outcome of infection. While host genotype explains most of the variation in immunological traits, parasite genotype explains most of the variation in parasitological traits, and both host and parasite genotypes impact immunopathology outcomes.

Indexed as

GenotypeMice, Inbred BALB CMice, Inbred C57BLSchistosoma mansoniSchistosomiasis mansoniAnimalsCytokinesFemaleHost-Parasite InteractionsMiceCytokinesBALB/c mouseC57BL/6 mouseHost-parasite interactionImmunopathogenesisSchistosoma mansoni

Identifiers

PMID38711063
PMCPMC11073996

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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.