Serum Proteomic Profile of Wild Stump-tailed Macaques (Macaca arctoides) Infected with Malaria Parasites in Thailand
Ontology highlight
ABSTRACT:
ORGANISM(S): Cellular Organisms
SUBMITTER: Sittiruk Roytrakul
PROVIDER: PXD039047 | JPOST Repository | Fri Dec 23 00:00:00 GMT 2022
REPOSITORIES: jPOST
Similar Datasets
Project description:In the rodent malaria parasite Plasmodium berghei, we found that an AP2 family transcription factor designated AP2-L plays a critical role in the development of the liver stage. Using DNA microarray analysis we showed that the expression of several genes, including those of parasitophorous vacuole membrane proteins, was significantly decreased in the early liver stage of AP2-L-depleted parasites. Gene expression of P. berghei liver stages was compared between wild type and AP2-L KO parasites. Liver stage parasites were cultured for 24h using HepG2 cells. Ten and seven biologically independent experiments were performed for wild type and AP2-L KO parasites, respectively.
2012-04-30 | E-GEOD-34877 | biostudies-arrayexpress
Project description:<p>Description:<br/> Experimental exposure to malaria parasites can lead to development of protective immunity, providing a foothold for the development of a malaria vaccine. The goal of this study is to investigate immune transcriptional profiles associated with malaria protective immune responses induced by experimental Chemo-Prophylaxis and Sporozoites (CPS) immunization of P. <i>falciparum</i>-naive human volunteers. Samples for this study were obtained from a CPS-immunization study conducted in 2011 (ClinicalTrials.gov Identifier: NCT01218893), where healthy volunteers received CPS-immunization with bites from different numbers of P. <i>falciparum</i>-infected mosquitoes (three times 15 (n=5), 10 (n=9) or 5 (n=10)). Five control subjects received uninfected mosquito bites under chloroquine prophylaxis. Fifteen weeks after discontinuation of chloroquine prophylaxis, all volunteers were challenged by exposure to infected mosquito bites. </p> <p>Study Design:<br/> A maximum of 30 volunteers were divided into four groups. All volunteers received weekly chloroquine prophylaxis for a period of 13 weeks (91 days). During these 13 weeks, on days 8, 36 and 64 they were exposed to the bites of 15 mosquitoes. Group 1 (n=5, positive control) received three CPS immunizations by 15 mosquitoes infected with P. falciparum sporozoites. Group 2 (n=10) received three times 10 bites from infected mosquitoes and 5 bites from uninfected mosquitoes. Group 3 (n=10) received three times 5 bites from infected mosquitoes and 10 bites from uninfected mosquitoes. Group 4 (n=5), the negative control, received three placebo immunizations with 15 bites of uninfected mosquitoes. Fifteen weeks after discontinuation of chloroquine prophylaxis, all 30 volunteers were challenged at day 196 by the bites of 5 infectious mosquitoes and followed for 21 days. All subjects were treated with chloroquine 21 days after challenge or whenever they had a positive thick smear during that period. </p>
| phs001346 | dbGaP
Project description:Sterile immunity to Plasmodium falciparum infection can be induced experimentally in humans after few exposures. An example is the induction of immunity using whole parasites by exposure of malaria-naive volunteers to infectious mosquito bites while using chloroquine prophylaxis (CPS immunization). Chloroquine kills blood-stage parasites but leaves liver-stage parasites unaffected, thereby exposing the liver-stage and early blood-stage antigens to the immune system. Upon subsequent challenge, volunteers are completely protected from infection, but protective efficacy decreases when fewer infectious mosquito bites are used for CPS immunization. Efforts to understand the mechanisms of this immunity, and how it differs from naturally-acquired immunity, may provide critical insights that could aid malaria vaccine development. In this pilot study, transcriptomic features are derived from blood samples collected before and after challenge with infectious mosquito bites. 12 samples; paired pre- and post-challenge for 5 individuals, plus two controls
2013-09-18 | E-GEOD-50957 | biostudies-arrayexpress
Project description:Sterile immunity to Plasmodium falciparum infection can be induced experimentally in humans after few exposures. An example is the induction of immunity using whole parasites by exposure of malaria-naive volunteers to infectious mosquito bites while using chloroquine prophylaxis (CPS immunization). Chloroquine kills blood-stage parasites but leaves liver-stage parasites unaffected, thereby exposing the liver-stage and early blood-stage antigens to the immune system. Upon subsequent challenge, volunteers are completely protected from infection, but protective efficacy decreases when fewer infectious mosquito bites are used for CPS immunization. Efforts to understand the mechanisms of this immunity, and how it differs from naturally-acquired immunity, may provide critical insights that could aid malaria vaccine development. In this pilot study, transcriptomic features are derived from blood samples collected before and after challenge with infectious mosquito bites.
2013-09-18 | GSE50957 | GEO
Project description:CD4+ T cells are critical for defense against the Plasmodium parasites that cause malaria. To better understand CD4+ T cell effector mechanisms during malaria, we performed microarray analysis of CD4+ T cells from naïve and infected mice. Comparison of activated (CD44 hi CD62L lo) CD4+ T cells from infected mice to bulk CD4+ T cells from naïve mice revealed a subset of genes that were upregulated by infection with Plasmodium chabaudi. These results help generate a more complete picture of CD4+ T cell function in malaria.
2016-11-12 | GSE81196 | GEO
Project description:Background Histone deacetylase (HDACs) inhibitors are being intensively pursued as potential new antimalarial drugs, and are also emerging as valuable tools for investigating transcriptional control in malaria parasites. In this study, the genome-wide transcriptional effects of three structurally related hydroxamate HDAC inhibitors were profiled in Plasmodium falciparum, the most lethal of the malaria parasite species that infects humans. Results Following 2h exposure to trichostatin A (TSA), suberoylanilide hydroxamic acid (SAHA) or a 2-aminosuberic acid derivative (2-ASA-9), ~18-28% of genes in P. falciparum trophozoite-stage parasites were regulated greater than two fold. This global induction was transitory, with fewer genes (3-5%) regulated after removing the compounds and culturing for a further 2h. Just nine genes, including alpha-II-tubulin, were up-regulated by all three compounds. Despite structural similarity, the three inhibitors caused quite diverse transcriptional effects, possibly reflecting subtle differences in mode of action or cellular distribution. Conclusions Three structurally related HDAC inhibitors have been found to cause profound, genome-wide, transcriptional changes in P. falciparum parasites, but most effects were transitory. This highlights the dynamic and exquisitely controlled nature of transcription in these malaria parasites. We also identified a small subset of nine genes over-expressed by all three HDAC inhibitors that may represent the first recognized set of transcriptional markers that signify HDAC inhibition in malaria parasites. This data set is an important contribution to our understanding of gene regulation in malaria parasites and supports growing evidence for the potential of HDAC inhibitors as new antimalarial agents.
2012-05-01 | GSE25642 | GEO
Project description:After entering their mammalian host via the bite of an Anopheles mosquito, Plasmodium sporozoites migrate to the liver where they traverse several hepatocytes before invading the one inside which they will develop and multiply into thousands of merozoites. Although this constitutes an essential step in malaria infection, the requirements of Plasmodium parasites in liver cells and how they use the host cell for their own survival and development are poorly understood. To gain new insights into the molecular host-parasite interactions that take place during malaria liver infection, we have used high-throughput microarray technology to determine the transcriptional profile of P. yoelii-infected hepatocytes that were collected from P. yoelii-infected mice 24 and 40 h after infection. This in vivo microarray expression was compared with the microarray analysis of in vitro infected hepatoma cells infected with closely related rodent malaria parasite P. berghei. Differential expression patterns for host genes identify genes and pathways involved in the host response to rodent Plasmodium parasites. Keywords: gene expression
2010-02-24 | GSE14967 | GEO
Project description:In the rodent malaria parasite Plasmodium berghei, we found that an AP2 family transcription factor designated AP2-L plays a critical role in the development of the liver stage. Using DNA microarray analysis we showed that the expression of several genes, including those of parasitophorous vacuole membrane proteins, was significantly decreased in the early liver stage of AP2-L-depleted parasites. Gene expression of P. berghei sporozoites was compared between wild type and AP2-G KO parasites. Five biologically independent experiments were performed for each genotype.
2012-04-30 | E-GEOD-34806 | biostudies-arrayexpress
Project description:Malaria parasites rely on a plastid organelle for survival during the blood stages of infection. However, the entire organelle is dispensable as long as the isoprenoid precursor isopentenyl pyrophosphate (IPP) is supplemented in the culture medium. We engineered parasites to produce isoprenoid precursors from a mevalonate-dependent pathway, creating a parasite line that replicates normally after the loss of the apicoplast organelle. We show that carbon-labeled mevalonate is specifically incorporated into isoprenoid products, opening new avenues for researching this essential class of metabolites in malaria parasites. We also show that essential apicoplast proteins, such as the enzyme target of the drug fosmidomycin, can be deleted in this mevalonate bypass parasite line, providing a method to determine the roles of other important apicoplast-resident proteins. Several antibacterial drugs kill malaria parasites because they target basic processes, such as transcription, in the organelle. We used metabolomic and transcriptomic methods to characterize parasite metabolism after azithromycin treatment triggered loss of the apicoplast. These results provide insight into the effects of apicoplast-disrupting drugs, several of which have been used to treat malaria infections in humans. Overall, the mevalonate bypass system provides a way to probe essential aspects of apicoplast biology and study the effects of drugs that target apicoplast processes.
2020-02-11 | GSE136169 | GEO
Project description:Purpose: The goals of this study are to compare parasite transcriptomes in sickle cell trait infected red blood cells during the intraerythrocytic developmental cycle (IDC) from in vitro time series and in vivo blood samples to identify new therapeutic targets in the treatment of malaria Methods: In vitro time series: Parasites were synchronized to early ring-stage parasites and sampled every three hours for 48 hours to capture every stage of the IDC, generating 16 RNA-seq libraries per replicate (128 total). In vivo blood samples: Samples were collected in an observational study of malaria in children in Kenieroba, Mali (ClinicalTrials.gov Identifier: NCT02645604). From children presenting with uncomplicated falciparum malaria, we selected all available samples from children with HbAS and matched each of these to a sample from a child with HbAA on: month of episode, parasite density, ethnic background, and, if possible, ABO blood type.
2021-05-26 | GSE163144 | GEO