Correction to: Integrative analysis associates monocytes with insufficient erythropoiesis during acute Plasmodium cynomolgi malaria in rhesus macaques

Tang, Yan; Joyner, Chester J.; Cabrera-Mora, Mónica; Saney, Celia L.; Lapp, Stacey A.; Nural, Mustafa V.; Pakala, Suman B.; DeBarry, Jeremy D.; Soderberg, Stephanie R.; Kissinger, Jessica C.; Lamb, Tracey J.; Galinski, Mary R.; Styczynski, Mark P.

doi:10.1186/s12936-017-2134-z

Cited by 3 publications

(4 citation statements)

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“…Tang, et al . 81 integrated multiple data types from BM and peripheral blood to identify dysfunctional BM mechanisms during the E04 longitudinal P. cynomolgi -rhesus monkey infections. This work revealed significant alteration in the BM transcriptome, and inflammation pathways were enriched.…”

Section: Usage Notesmentioning

confidence: 99%

MaHPIC malaria systems biology data from Plasmodium cynomolgi sporozoite longitudinal infections in macaques

et al. 2022

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Plasmodium cynomolgi causes zoonotic malarial infections in Southeast Asia and this parasite species is important as a model for Plasmodium vivax and Plasmodium ovale. Each of these species produces hypnozoites in the liver, which can cause relapsing infections in the blood. Here we present methods and data generated from iterative longitudinal systems biology infection experiments designed and performed by the Malaria Host-Pathogen Interaction Center (MaHPIC) to delve deeper into the biology, pathogenesis, and immune responses of P. cynomolgi in the Macaca mulatta host. Infections were initiated by sporozoite inoculation. Blood and bone marrow samples were collected at defined timepoints for biological and computational experiments and integrative analyses revolving around primary illness, relapse illness, and subsequent disease and immune response patterns. Parasitological, clinical, haematological, immune response, and -omic datasets (transcriptomics, proteomics, metabolomics, and lipidomics) including metadata and computational results have been deposited in public repositories. The scope and depth of these datasets are unprecedented in studies of malaria, and they are projected to be a F.A.I.R., reliable data resource for decades.

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Section: Usage Notesmentioning

confidence: 99%

MaHPIC malaria systems biology data from Plasmodium cynomolgi sporozoite longitudinal infections in macaques

et al. 2022

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“…Infusion of MSCs was also found to enhance the expression of GATA-1. GATA-1, commonly referred to as a master transcription factor of the erythroid lineage, plays an important role in the differentiation of BFU-E to CFU-E, which is facilitated by the mediator subunit MED1/TRAP220 [ 7 – 9 ]. By performing in vitro studies, it has been observed that MED1/TRAP220 binds to GATA factors that forms a bridge between these transcription factors and the RNA polymerase II machinery [ 7 ].…”

Section: Mesenchymal Stem Cells (Mscs) As An Immunotherapy For Malariamentioning

confidence: 99%

“…Additionally, tissue deposition of haemozoin, a byproduct of haemoglobin digestion formed in the haem detoxification process has been linked to malarial anaemia and dyserythropoiesis. Moreover, the proliferation and differentiation of erythroid progenitors are also impaired during malaria infection due to reduced expression of erythroid-specific transcription factors such as GATA-1 and GATA-2 [ 7 – 9 ]. GATA-1, a key transcription factor for erythroid cell development, facilitates the survival and late-stage differentiation of erythroid precursors, whereas GATA-2 is critical for the maintenance and proliferation of haematopoietic progenitors.…”

Section: Introductionmentioning

confidence: 99%

Mesenchymal Stem Cells: A Novel Therapeutic Approach to Enhance Protective Immunomodulation and Erythropoietic Recovery in Malaria

Kalkal

Tiwari

Thakur

et al. 2021

Stem Cell Rev and Rep

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Graphical Abstract Mesenchymal stem cells (MSCs) are self-renewing, multi-potent heterogeneous stem cells that display strong tissue protective and restorative properties by differentiating into cells of the mesodermal lineages. In addition to multi-lineage differentiation capacity, MSCs play important roles in regulating immune responses, inflammation, and tissue regeneration. MSCs play a role in the outcome of the pathogenesis of several infectious diseases. A unique subset of MSCs accumulates in secondary lymphoid organs during malaria disease progression. These MSCs counteract the capacity of malaria parasites to subvert activating co-stimulatory molecules and to regulate expression of negative co-stimulatory molecules on T lymphocytes. Consequently, MSCs have the capacity to restore the functions of CD34 + haematopoietic cells and CD4 + and CD8 + T cells during malaria infection. These observations suggest that cell-based therapeutics for intervention in malaria may be useful in achieving sterile clearance and preventing disease reactivation. In addition, MSCs provide host protection against malaria by reprogramming erythropoiesis through accelerated formation of colony-forming-units-erythroid (CFU-E) cells in the bone marrow. These findings suggest that MSCs are positive regulators of erythropoiesis, making them attractive targets for treatment of malarial anemia. MSC-based therapies, unlike anti-malarial drugs, display therapeutic effects by targeting a large variety of cellular processes rather than a single pathway. In the present review we focus on these recent research findings and discuss clinical applications of MSC-based therapies for malaria.

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“…Concealment of a non-circulating infected RBC sub-population from the peripheral circulation during P. cynomolgi infection of M. mulatta was also shown, which may be an important aspect of the host-pathogen relationship ( Fonseca et al., 2017 ). Furthermore, using systems analysis to model the alterations in cell populations in the bone marrow during P. cynomolgi infection of M. mulatta led to the hypothesis that malarial anemia may be driven by monocyte-associated disruption of the GATA-1/GATA-2 in erythroid progenitors resulting in insufficient erythropoiesis during acute infection ( Tang et al., 2017 ).…”

Section: Introductionmentioning

confidence: 99%

Parasite-Host Interaction and Pathophysiology Studies of the Human Relapsing Malarias Plasmodium vivax and Plasmodium ovale Infections in Non-Human Primates

Pasini

Kocken

2021

Front. Cell. Infect. Microbiol.

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Malaria remains a serious health concern across the globe. Historically neglected, non-Falciparum human malarias were put back on the agenda by a paradigm shift in the fight against malaria from malaria control to malaria eradication. Here, we review the modeling of the relapsing parasites Plasmodium vivax (P. vivax) and Plasmodium ovale (P. ovale) in non-human primates with a specific focus on the contribution of these models to our current understanding of the factors that govern parasite-host interactions in P. vivax and P. ovale parasite biology and pathophysiology.

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Correction to: Integrative analysis associates monocytes with insufficient erythropoiesis during acute Plasmodium cynomolgi malaria in rhesus macaques

Cited by 3 publications

References 1 publication

MaHPIC malaria systems biology data from Plasmodium cynomolgi sporozoite longitudinal infections in macaques

MaHPIC malaria systems biology data from Plasmodium cynomolgi sporozoite longitudinal infections in macaques

Mesenchymal Stem Cells: A Novel Therapeutic Approach to Enhance Protective Immunomodulation and Erythropoietic Recovery in Malaria

Parasite-Host Interaction and Pathophysiology Studies of the Human Relapsing Malarias Plasmodium vivax and Plasmodium ovale Infections in Non-Human Primates

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