E-MTAB-4791
Ontology highlight
ABSTRACT:
PROVIDER: E-MTAB-4791 | ExpressionAtlas | 2016-06-06
REPOSITORIES: ExpressionAtlas
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| E-MTAB-4791-analysis-methods.tsv | Tabular | |||
| E-MTAB-4791-atlasExperimentSummary.Rdata | Rdata | |||
| E-MTAB-4791-configuration.xml | Xml | |||
| E-MTAB-4791-percentile-ranks.tsv | Tabular | |||
| E-MTAB-4791.condensed-sdrf.tsv | Tabular |
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2016-10-01 | E-MTAB-4791 | biostudies-arrayexpress
Project description:Hypoglycemia is a clinical hallmark of severe malaria, the often-lethal outcome of Plasmodium falciparum infection. Yet, the underlying mechanisms driving the pathogenesis of malaria-associated hypoglycemia remain poorly understood. Here we report that labile heme, an alarmin generated as a byproduct of hemolysis during the blood stage of Plasmodium spp. infection, plays a central role in the development of malaria-associated hypoglycemia. Labile heme recapitulated the hypometabolic response to Plasmodium (chabaudi chabaudi; Pcc) infection in mice, including the development of anorexia, transcriptional repression of hepatic glucose production (HGP) and reduction of glycemia, energy expenditure (EE) as well as core body temperature. While this hypometabolic response is protective against immune-mediated liver damage and anemia, when sustained over time it can lead to hypoglycemia and compromise EE as well as thermoregulation. In response, asexual stages of Plasmodium spp. activate a transcriptional program that reduces virulence in favor of sexual commitment and presumably malaria transmission. In conclusion, malaria-associated hypoglycemia represents a trade-off of a hypometabolic defense strategy against Plasmodium infection.
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Project description:Hypoglycemia is a clinical hallmark of severe malaria, the often-lethal outcome of Plasmodium falciparum infection. Yet, the underlying mechanisms driving the pathogenesis of malaria-associated hypoglycemia remain poorly understood. Here we report that labile heme, an alarmin generated as a byproduct of hemolysis during the blood stage of Plasmodium spp. infection, plays a central role in the development of malaria-associated hypoglycemia. Labile heme recapitulated the hypometabolic response to Plasmodium (chabaudi chabaudi; Pcc) infection in mice, including the development of anorexia, transcriptional repression of hepatic glucose production (HGP) and reduction of glycemia, energy expenditure (EE) as well as core body temperature. While this hypometabolic response is protective against immune-mediated liver damage and anemia, when sustained over time it can lead to hypoglycemia and compromise EE as well as thermoregulation. I response, asexual stages of Plasmodium spp. activate a transcriptional program that reduces virulence in favor of sexual commitment and presumably malaria transmission. In conclusion, malaria-associated hypoglycemia represents a trade-off of a hypometabolic defense strategy against Plasmodium infection.
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Project description:A major obstacle in deciphering the hepatic stage of the malaria parasite has been the challenges associated with culturing the infected hepatocytes through the entire liver stage cycle, including that of the dormant form known as hypnozoites. Primary hepatocytes lose their specialized functions in long-term in vitro culture. Hepatocyte infection represents the first step for clinically silent infection and development of malaria parasite Plasmodium in the liver. Thus this liver stage is an ideal target for development of novel antimalarial drugs and vaccine. However, drug discovery against Plasmodium liver stage is severely hampered by the poor understanding of host-cell and parasites interactions during the liver stage infection and development. In this study, we have performed tandem mass tags (TMT) labelling based quantitative proteomic analysis in simian primary hepatocytes cultured in three different systems of susceptibility to plasmodium infection. Our results represent the first documentation of potentially essential molecular markers including asialoglycoprotein receptor (ASGPR), apolipoproteins, squalene synthase and scavenger receptor B1 (SR-BI) required for productive infection and full development in relapsing Plasmodium species. The identification of these candidate proteins for constructive infection and development of Plasmodium in malaria paves the way to explore them as therapeutic targets.
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