Plasmodium yoelii Erythrocyte Binding-like Protein Modulates Host Cell Membrane Structure, Immunity, and Disease Severity
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ABSTRACT:
PROVIDER: PRJNA549076 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9307520.fastq.gz | Fastqsanger.gz | |||
| SRR9307530_1.fastq.gz | Fastqsanger.gz | |||
| SRR9307530_2.fastq.gz | Fastqsanger.gz | |||
| SRR9307521.fastq.gz | Fastqsanger.gz | |||
| SRR9307531_1.fastq.gz | Fastqsanger.gz |
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Project description:Erythrocyte binding-like (EBL) proteins are known to play an important role in malaria parasite invasion; however, any roles in regulating host immune responses remain unknown. Here we show that an amino acid substitution (C741Y) in the protein trafficking domain of Plasmodium yoelii EBL (PyEBL) changes host immune response and disease severity, but not invasion of red blood cells (RBCs) as suggested previously. The C741Y substitution alters protein processing and trafficking in merozoites and in the cytoplasm of iRBCs, reduces its binding to Band 3, increases phosphatidylserine (PS) surface exposure, and elevates osmotic fragility of iRBCs. The modified iRBC surface triggers PS-CD36 mediated phagocytosis of iRBCs, host type I interferon (IFN-I) signaling, and T cell differentiation, leading to improved host survival. This study reveals a previously unknown role of PyEBL in regulating the innate immune response and host-pathogen interaction, which may be explored for developing disease control strategies.
2019-11-29 | GSE132796 | GEO
Project description:Plasmodium yoelii yoelii Epigenomics
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Project description:Plasmodium yoelii yoelii Genome sequencing
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Project description:Plasmodium yoelii yoelii Transcriptome or Gene expression
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Project description:Plasmodium yoelii yoelii strain:17XNL Genome sequencing and assembly
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Project description:Plasmodium yoelii YM asexual blood stage parasites express multiple members of the py235 gene family, part of the super-family of genes including those coding for Plasmodium vivax reticulocyte binding proteins and Plasmodium falciparum RH proteins. Dr Tony Holder's laboratory (NIMR, London) has been successful in deleting one of the RH family genes (Py01365) by transfection and insertion of the TgDHFR gene, and cloned the resulting parasite in YM background. The gene expression patterns of the mutant parasite line were compared to that of the wild type YM parasite.
2011-04-25 | E-MTAB-636 | biostudies-arrayexpress
Project description:Erythrocyte-binding-like (EBL) proteins are known to play an important role in malaria parasite invasion of red blood cells (RBCs); however, any roles of EBL proteins in regulating host immune responses remain unknown. Here, we show that Plasmodium yoelii EBL (PyEBL) can shape disease severity by modulating the surface structure of infected RBCs (iRBCs) and host immune responses. We identified an amino acid substitution (a change of C to Y at position 741 [C741Y]) in the protein trafficking domain of PyEBL between isogenic P. yoelliinigeriensis strain N67 and N67C parasites that produce different disease phenotypes in C57BL/6 mice. Exchanges of the C741Y alleles altered parasite growth and host survival accordingly. The C741Y substitution also changed protein processing and trafficking in merozoites and in the cytoplasm of iRBCs, reduced PyEBL binding to band 3, increased phosphatidylserine (PS) surface exposure, and elevated the osmotic fragility of iRBCs, but it did not affect invasion of RBCs in vitro The modified iRBC surface triggered PS-CD36-mediated phagocytosis of iRBCs, host type I interferon (IFN-I) signaling, and T cell differentiation, leading to improved host survival. This study reveals a previously unknown role of PyEBL in regulating host-pathogen interaction and innate immune responses, which may be explored for developing disease control strategies.IMPORTANCE Malaria is a deadly parasitic disease that continues to afflict hundreds of millions of people every year. Infections with malaria parasites can be asymptomatic, with mild symptoms, or fatal, depending on a delicate balance of host immune responses. Malaria parasites enter host red blood cells (RBCs) through interactions between parasite ligands and host receptors, such as erythrocyte-binding-like (EBL) proteins and host Duffy antigen receptor for chemokines (DARC). Plasmodium yoelii EBL (PyEBL) is known to play a role in parasite invasion of RBCs. Here, we show that PyEBL also affects disease severity through modulation of host immune responses, particularly type I interferon (IFN-I) signaling. This discovery assigns a new function to PyEBL and provides a mechanism for developing disease control strategies.
| S-EPMC6946805 | biostudies-literature
Project description:Plasmodium yoelii YM asexual blood stage parasites express multiple members of the py235 gene family, part of the super-family of genes including those coding for Plasmodium vivax reticulocyte binding proteins and Plasmodium falciparum RH proteins. Dr Tony Holder's laboratory (NIMR, London) has been successful in deleting one of the RH family genes (Py01365) by transfection and insertion of the TgDHFR gene, and cloned the resulting parasite in YM background. The gene expression patterns of the mutant parasite line were compared to that of the wild type YM parasite. ArrayExpress Release Date: 2011-04-25 Publication Title: Targeted Disruption of py235ebp-1: Invasion of Erythrocytes by Plasmodium yoelii Using an Alternative Py235 Erythrocyte Binding Protein Publication Author List: Solabomi A. Ogun, Rita Tewari, Thomas D. Otto, Steven A. Howell, Ellen Knuepfer, Deirdre A. Cunningham, Zhengyao Xu, Arnab Pain, Anthony A. Holder Person Roles: submitter Person Last Name: Service Person First Name: Submission Person Mid Initials: Person Email: datahose@sanger.ac.uk Person Phone: Person Address: The Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridgeshire, CB10 1SA, United Kingdom Person Affiliation: Wellcome Trust Sanger Institute Person Roles: investigator Person Last Name: Holder Person First Name: Anthony Person Mid Initials: A Person Email: aholder@nimr.mrc.ac.uk Person Phone: Person Address: Division of Parasitology, MRC National Institute for Medical Research, London, UK Person Affiliation: MRC National Institute for Medical Research Person Roles: Project Coordinator Person Last Name: Sanders Person First Name: Mandy Person Mid Initials: J Person Email: mjs@sanger.ac.uk Person Phone: 01223 834244 Person Address: Wellcome Trust Genome Campus,Hinxton,Cambridge. CB10 1SA UK Person Affiliation: Wellcome Trust Sanger Institute
2011-07-14 | GSE30620 | GEO