Mus musculus
Ontology highlight
ABSTRACT:
OTHER RELATED OMICS DATASETS IN: E-GEOD-4324
PROVIDER: PRJNA94747 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The goal of this study was to examine whether immune responses to Plasmodium chabaudi infection differ between the sexes and are altered by the presence of gonadal steroids. Gonadally-intact males were more likely than intact females to die following P. chabaudi infection, exhibit slower recovery from infection-associated weight loss, hypothermia, and anemia, have reduced IFNγ-associated gene expression and IFNγ production during peak parasitemia, and produce less antibody during the recovery phase of infection. Gonadectomy of male and female mice altered these sex-associated differences, suggesting that sex steroid hormone, in particular androgens and estrogens, may modulate immune responses to infection. Keywords: Time Course
2006-06-01 | GSE4324 | GEO
Project description:The goal of this study was to examine whether immune responses to Plasmodium chabaudi infection differ between the sexes and are altered by the presence of gonadal steroids. Gonadally-intact males were more likely than intact females to die following P. chabaudi infection, exhibit slower recovery from infection-associated weight loss, hypothermia, and anemia, have reduced IFNγ-associated gene expression and IFNγ production during peak parasitemia, and produce less antibody during the recovery phase of infection. Gonadectomy of male and female mice altered these sex-associated differences, suggesting that sex steroid hormone, in particular androgens and estrogens, may modulate immune responses to infection. Experiment Overall Design: Intact and gonadectomized (gdx) male and female C57BL/6 mice were inoculated with 106 P. chabaudi AS-infected erythrocytes and responses to infection were monitored. For microarray analyses, RNA was isolated from 5 x 106 white blood cells (WBCs) that were isolated from spleens 0, 3, 7, or 14 days after inoculation with P. chabaudi. Equivalent aliquots of RNA from 3 animals/treatment group were pooled and 3 separate pools were processed on separate Affymetrix GeneChips (n = 3 GeneChips/time point/treatment group).
2008-11-22 | E-GEOD-4324 | biostudies-arrayexpress
Project description:Transcription profiling by array of mice infected with Plasmodium chabaudi after gonadectomization to investigate involvement of gonadal steroids
2014-08-29 | E-GEOD-4324 | ExpressionAtlas
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.
2021-12-31 | E-MTAB-10935 | 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. 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.
2021-12-31 | E-MTAB-10939 | biostudies-arrayexpress
Project description:In order to gain a better understanding of gene expression during early malaria infection, we conducted microarray analysis of early blood responses in mice infected with erythrocytic stage Plasmodium chabaudi. Immediately following infection, we observed coordinated and sequential waves of immune responses, with interferon-associated gene transcripts dominating by 16 hours post-infection, followed by strong increases in natural killer (NK) cell-associated and MHC class I-related transcripts by 32 hours post-infection. We hypothesized that the observed elevation in NK cell-associated transcripts could be the result of a dramatic increase in the proportion of NK cells in the blood during infection, which we confirmed by flow cytometry. Subsequent microarray analysis of NK cells isolated from the peripheral blood of infected mice revealed a cell proliferation expression signature consistent with the observation that NK cells replicate in response to infection. Early proliferation of NK cells was directly observed in studies with adoptively transferred cells in infected mice. These data indicate that the early response to P. chabaudi infection of the blood is marked by a primary wave of interferon with a subsequent response by NK cells. Keywords: murine NK cell response to Plasmodium chabaudi infection We analyzed a series of 10 MEEBO arrays on which were hybed RNA amplified from NK cells of C57BL/6 mice either mock-infected or infected with P. chabaudi AS.
2010-05-19 | E-GEOD-12727 | biostudies-arrayexpress
Project description:In order to gain a better understanding of gene expression during early malaria infection, we conducted microarray analysis of early blood responses in mice infected with erythrocytic stage Plasmodium chabaudi. Immediately following infection, we observed coordinated and sequential waves of immune responses, with interferon-associated gene transcripts dominating by 16 hours post-infection, followed by strong increases in natural killer (NK) cell-associated and MHC class I-related transcripts by 32 hours post-infection. We hypothesized that the observed elevation in NK cell-associated transcripts could be the result of a dramatic increase in the proportion of NK cells in the blood during infection, which we confirmed by flow cytometry. Subsequent microarray analysis of NK cells isolated from the peripheral blood of infected mice revealed a cell proliferation expression signature consistent with the observation that NK cells replicate in response to infection. Early proliferation of NK cells was directly observed in studies with adoptively transferred cells in infected mice. These data indicate that the early response to P. chabaudi infection of the blood is marked by a primary wave of interferon with a subsequent response by NK cells. Keywords: murine whole blood response to Plasmodium chabaudi infection We analyzed a series of 36 MEEBO arrays on which were hybed RNA amplified from whole blood of C57BL/6 mice either mock-infected or infected with P. chabaudi AS.
2010-05-19 | E-GEOD-12249 | biostudies-arrayexpress
Project description:In order to gain a better understanding of gene expression during early malaria infection, we conducted microarray analysis of early blood responses in mice infected with erythrocytic stage Plasmodium chabaudi. Immediately following infection, we observed coordinated and sequential waves of immune responses, with interferon-associated gene transcripts dominating by 16 hours post-infection, followed by strong increases in natural killer (NK) cell-associated and MHC class I-related transcripts by 32 hours post-infection. We hypothesized that the observed elevation in NK cell-associated transcripts could be the result of a dramatic increase in the proportion of NK cells in the blood during infection, which we confirmed by flow cytometry. Subsequent microarray analysis of NK cells isolated from the peripheral blood of infected mice revealed a cell proliferation expression signature consistent with the observation that NK cells replicate in response to infection. Early proliferation of NK cells was directly observed in studies with adoptively transferred cells in infected mice. These data indicate that the early response to P. chabaudi infection of the blood is marked by a primary wave of interferon with a subsequent response by NK cells. Keywords: murine whole blood response to Plasmodium chabaudi infection
2008-10-01 | GSE12249 | GEO
Project description:In order to gain a better understanding of gene expression during early malaria infection, we conducted microarray analysis of early blood responses in mice infected with erythrocytic stage Plasmodium chabaudi. Immediately following infection, we observed coordinated and sequential waves of immune responses, with interferon-associated gene transcripts dominating by 16 hours post-infection, followed by strong increases in natural killer (NK) cell-associated and MHC class I-related transcripts by 32 hours post-infection. We hypothesized that the observed elevation in NK cell-associated transcripts could be the result of a dramatic increase in the proportion of NK cells in the blood during infection, which we confirmed by flow cytometry. Subsequent microarray analysis of NK cells isolated from the peripheral blood of infected mice revealed a cell proliferation expression signature consistent with the observation that NK cells replicate in response to infection. Early proliferation of NK cells was directly observed in studies with adoptively transferred cells in infected mice. These data indicate that the early response to P. chabaudi infection of the blood is marked by a primary wave of interferon with a subsequent response by NK cells. Keywords: murine NK cell response to Plasmodium chabaudi infection
2008-10-01 | GSE12727 | GEO
Project description:Microarray profiling of whole blood of immunodeficient mouse strains at 24h after infection with Plasmodium chabaudi.
2012-11-19 | GSE23565 | GEO