Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Toxoplasma gondii infection and chronic IL-1 elevation drive hippocampal DNA double-strand break signaling, leading to cognitive deficits

ABSTRACT: Chronic inflammation, resulting from infections, is characterized by increased levels of cytokines including interleukin-1 (IL-1), but little is known about how IL-1 contributes to cognitive impairment, potentially via epigenetic processes. Here we demonstrate that mice chronically infected with the parasite Toxoplasma gondii exhibit impaired spatial memory, which is dependent on neuronal IL-1 signaling and mimicked by chronic exposure to IL-1beta. Both T. gondii infection and chronic IL-1beta drive H2A.X-dependent DNA double-strand break signaling in hippocampal neurons and invalidating neuronal H2A.X-dependent signaling blocks memory impairments caused by either exposure. Our results highlight the instrumental role of cytokine-induced double-strand-break-dependent signaling in spatial memory defects, which may be relevant to multiple brain diseases.

ORGANISM(S): Mus musculus

PROVIDER: GSE274667 | GEO | 2025/07/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Toxoplasma gondii infection and chronic IL-1 elevation drive hippocampal DNA double-strand break signaling, leading to cognitive deficits

Project description:Chronic inflammation, resulting from infections, is characterized by increased levels of cytokines including interleukin-1 (IL-1), but little is known about how IL-1 contributes to cognitive impairment, potentially via epigenetic processes. Here we demonstrate that mice chronically infected with the parasite Toxoplasma gondii exhibit impaired spatial memory, which is dependent on neuronal IL-1 signaling and mimicked by chronic exposure to IL-1beta. Both T. gondii infection and chronic IL-1beta drive H2A.X-dependent DNA double-strand break signaling in hippocampal neurons and invalidating neuronal H2A.X-dependent signaling blocks memory impairments caused by either exposure. Our results highlight the instrumental role of cytokine-induced double-strand-break-dependent signaling in spatial memory defects, which may be relevant to multiple brain diseases.

2025-07-30 | GSE274075 | GEO

Toxoplasma gondii infection and chronic IL-1 elevation drive hippocampal DNA double-strand break signaling, leading to cognitive deficits

Project description:Toxoplasma gondii infection and chronic IL-1 elevation drive hippocampal DNA double-strand break signaling, leading to cognitive deficits

| PRJNA1144902 | ENA

Toxoplasma gondii infection and chronic IL-1 elevation drive hippocampal DNA double-strand break signaling, leading to cognitive deficits

Project description:Toxoplasma gondii infection and chronic IL-1 elevation drive hippocampal DNA double-strand break signaling, leading to cognitive deficits

| PRJNA1147622 | ENA

Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice

Project description:Neutrophil abscess formation is critical in innate immunity against many pathogens. Here, the mechanism of neutrophil abscess formation was investigated using a mouse model of Staphylococcus aureus cutaneous infection. Gene expression analysis of S. aureus-infected skin revealed that induction of neutrophil recruitment genes was largely dependent upon IL-1beta/IL-1R activation. Unexpectedly, using IL 1beta reporter mice, neutrophils were identified as the primary source of IL-1beta at the site of infection. Furthermore, IL-1beta-producing neutrophils were necessary and sufficient for abscess formation and bacterial clearance. S. aureus-induced IL 1beta production by neutrophils required TLR2, NOD2, FPRs and the ASC/NLRP3 inflammasome. Taken together, IL-1beta and neutrophil abscess formation during an infection are functionally, spatially and temporally linked as a consequence of direct IL-1beta production by neutrophils.

2012-12-05 | GSE36826 | GEO

Transcriptional profiling of hypoxic cells and identification of HEXIM1-dependent genes.

Project description:To identify primary response genes (PRGs) that were differently expressed within 1 hr of hypoxia exposure, we performed global transcriptional profiling using the Agilent Technologies SurePrint G3 Human GE Microarray . To identify Hexim1-dependent genes, we compare profiles of hypoxia PRGs in cells transfected with control or Hexim1 targeting double-strand siRNA HeLa cells were transfected with control and HEXIM1-targeted double-strand siRNA and 48 hr after treated with IL-1beta in combination with normoxia or hypoxia (5% CO2, 0.5% O2, balanced with N2) O for 1 hr.

2012-09-21 | E-GEOD-41023 | biostudies-arrayexpress

Neutrophil-derived IL-1β is sufficient for abscess formation in immunity against Staphylococcus aureus in mice

2012-12-05 | E-GEOD-36826 | biostudies-arrayexpress

Reconstitution of SPO11-dependent double-strand break formation

Project description:Reconstitution of SPO11-dependent double-strand break formation

| PRJNA1150203 | ENA

Gene expression data of interleukin-7-dependent and BCR-ABL1-transformed pre-B cells

Project description:This analysis focused on identifying factors that protect pre-B cells against DNA double strand break (DSB)-mediated DNA damage stress during pre-B cell differentiation. Differentiation of pre-B cells including immunoglobulin light chain gene recombination were performed by withdrawal of interleukin-7 (IL-7) from IL-7-dependent murine pre-B cells or by inhibition of the BCR-ABL1 kinase activity in BCR-ABL1-transformed pre-B cells. The BCR-ABL1 kinase inhibitor STI571 (Imatinib) was used for the inhibition of BCR-ABL1. IL-7-dependent murine pre-B cells were either cultured in IL-7 (10 ng/ml) or induced to differentiate by withdrawal of IL-7. BCR-ABL1-transformed pre-B cells were either treated with 10 ÂµM STI571 (in absence or presence of 10 ng/ml IL-7) for 16 hours or cultured without STI571. Three samples for each condition were processed.

2010-05-27 | E-GEOD-21664 | biostudies-arrayexpress

Identification of IL-22 regulated genes in the ileum after infection with Toxoplasma gondii

Project description:IL-22 acts on epithelial cells and has been shown to induce tissue protective and wound healing responses in these cells. But it has recently been decribed that IL-22 exacerbates ileatis after infection with T. gondii. The goal of the study is to identify the IL-22-dependent genes during T. gondii infection in order to understand why IL-22 is pathogenic in this context. one experimental condition, 5 mice per group, 2 groups: WT and IL-22 KO animals

2015-01-31 | E-GEOD-65472 | biostudies-arrayexpress

Transcriptional profile of brain TRM in Toxoplasma gondii infection

Project description:During chronic infection memory T cells acquire a unique phenotype and become dependent on different survival signals than those needed for memory T cells generated during an acute infection. The distinction between the role of effector and memory T cells in an environment of persistent antigen remains unclear. Here, in the context of chronic Toxoplasma gondii infection we demonstrate that a population of CD8 T cells exhibiting a tissue resident memory (TRM) phenotype persists in the brain. We show that this population is distributed throughout the brain in both parenchymal and extraparenchymal spaces. Furthermore, this population is transcriptionally distinct and exhibits a transcriptional signature consistent with the TRM observed in acute viral infections.

2017-06-12 | GSE95105 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data