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Series GSE266399 Query DataSets for GSE266399
Status Public on May 03, 2024
Title Cytoadhesion of Plasmodium falciparum-infected red blood cells changes the expression of cytokine-, histone- and antiviral protein-encoding genes in brain endothelial cells
Organism Homo sapiens
Experiment type Expression profiling by high throughput sequencing
Summary Introduction Malaria remains a significant global health problem, particularly due to the human malaria parasite Plasmodium falciparum, which is responsible for most fatal infections. Infected red blood cells (iRBCs) evade spleen clearance by adhering to endothelial cells (ECs), triggering capillary blockage, inflammatory cytokine release, endothelial dysfunction, and altered vascular permeability, prompting an endothelial transcriptional response. Methods The iRBCIT4var04/HBEC-5i model, where iRBCs present IT4var04 (VAR2CSA) on their surface was employed to analyse the effects of iRBC binding on ECs. We used this model to investigate how cytoadhesion of iRBCs to ECs influences their expression profile depending on the temperature (37°C vs 40°C). Results Binding of non-infected RBCs (niRBCs) and fever alone significantly changes expression of hundreds of genes in ECs. Comparing the expression profile of HBEC-5i cultured either in the presence of iRBCs or in the presence of niRBCs, genes encoding proteins assigned to the GO terms immune response, nucleosome assembly, NF-kappa B signaling, angiogenesis, and antiviral immune response/interferon-alpha/beta signaling pathway were significantly up-regulated. If the cultivation temperature is increased from 37°C to 40°C, which simulates fever, a further significant increase in expression can be observed for most regulated genes, especially for genes coding for cytokines and proteins involved in angiogenesis. Conclusion The presence of iRBCs leads to the stimulation of ECs, activating several immunological signaling pathways and affecting antiviral (-parasitic) mechanisms and angiogenesis. Furthermore, to our knowledge, the induction of the interferon-alpha/beta signaling pathway in ECs in response to iRBCs has been described for the first time.
 
Overall design The iRBCIT4var04/HBEC-5i model, where Plasmodium falciparum infected red blood cells (iRBC) present IT4var04 (VAR2CSA) on their surface was employed to analyse the effects of iRBC binding on endothelial cells (ECs). We used this model to investigate how cytoadhesion of iRBCs to ECs influences their expression profile depending on the temperature (37°C vs 40°C).
 
Contributor(s) Allweier J, Bartels M, Torabi H, Martinez MT, Metwally N, Roeder T, Gutsmann T, Bruchhaus I
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Submission date May 01, 2024
Last update date May 03, 2024
Contact name Johannes Allweier
E-mail(s) johannes.allweier@bnitm.de
Organization name Bernhard Nocht Institute for Tropical Medicine
Street address Bernhard-Nocht-Straße 74
City Hamburg
ZIP/Postal code 20359
Country Germany
 
Platforms (1)
GPL20301 Illumina HiSeq 4000 (Homo sapiens)
Samples (15)
GSM8246398 01_Control
GSM8246399 02_Control
GSM8246400 04_Control
Relations
BioProject PRJNA1106906

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE266399_ExpressionBrowser.xlsx 26.1 Mb (ftp)(http) XLSX
SRA Run SelectorHelp
Raw data are available in SRA

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