Intestinal response to prenatal inflammation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA579380 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10343019_1.fastq.gz | Fastqsanger.gz | |||
| SRR10343019_2.fastq.gz | Fastqsanger.gz | |||
| SRR10343020_1.fastq.gz | Fastqsanger.gz | |||
| SRR10343020_2.fastq.gz | Fastqsanger.gz | |||
| SRR10343021_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 80 |
Similar Datasets
Project description:Chorioamnionitis (CA), resulting from intra-amniotic inflammation, is a frequent cause of preterm birth and exposes the immature intestine to bacterial toxins and/or inflammatory mediators before birth via fetal swallowing. This may affect intestinal immune development, interacting with the effects of enteral feeding and gut microbiota colonization just after birth. Using preterm pigs as model for preterm infants, we hypothesized that prenatal exposure to gram-negative endotoxin influences postnatal bacterial colonization and gut immune development. Pig fetuses were given intra-amniotic lipopolysaccharide (LPS) 3 d before preterm delivery by cesarean section, and were compared with litter-mate controls (CON) at birth and after 5 d of formula feeding and spontaneous bacterial colonization. Amniotic fluid was collected for analysis of leukocyte counts and cytokines, and the distal small intestine was analyzed for endotoxin level, morphology and immune cell counts. Intestinal gene expression and microbiota were analyzed by transcriptomics and metagenomics, respectively. At birth, LPS-exposed pigs showed higher intestinal endotoxin, neutrophil/macrophage density and shorter villi. About 1.0% of intestinal genes were affected at birth and DMBT1, a regulator of mucosal immune defense, was identified as the hub gene in the co-expression network. Genes related to innate immune response (TLR2, LBP, CD14, C3, SFTPD), neutrophil chemotaxis (C5AR1, CSF3R, CCL5) and antigen processing (MHC II, CD4) were also affected and expression levels correlated with intestinal neutrophil/macrophage density and amniotic fluid cytokine levels. On day 5, LPS and CON pigs showed similar necrotizing enterocolitis (NEC) lesions, endotoxin levels, morphology, immune cell counts, gene expressions and microbiota (except for difference in some low-abundant species). Our results show that CA markedly affects intestinal genes at preterm birth, including genes related to immune cell infiltration. However, a few days later, following the physiological adaptations to preterm birth, CA had limited effects on intestinal structure, function, gene expression, bacterial colonization and NEC sensitivity. We conclude that short-term, prenatal intra-amniotic inflammation is unlikely to exert marked effects on intestinal immune development in preterm neonates beyond the immediate neonatal period.
2019-10-25 | GSE139366 | GEO
Project description:Postnatal gut immunity and microbiota development is minimally affected by prenatal inflammation in preterm pigs
| PRJEB34982 | ENA
Project description:Postnatal gut immunity and microbiota development is minimally affected by prenatal inflammation in preterm pigs
| PRJEB35052 | ENA
Project description:This study uses whole-genome bisulfite sequencing to characterize the methylomes of the AOM/DSS mouse model at single-base resolution. In this model, mice are treated with dextran sodium sulfate (DSS) to induce colitis. When this treatment is preceded by injections of the weak carcinogen azoxymethane (AOM) the mice develop intestinal tumors. Our results identify hypermethylated DMVs as a prominent feature of the colitis methylome that is conserved in intestinal adenocarcinomas. Further analyses reveal a subset of DMV-associated genes, expressed in normal intestinal epithelial cells, that were silenced and hypermethylated in inflamed and cancerous intestinal cells. Together, these findings provide strong support for the hypothesis that inflammatory signals induce a higher risk for cancer development by manipulating the epigenome. . Whole genome methylation analysis of M. musculus. Three conditions were sequenced analyzed, the first is an untreated control, the second corresponds to inflammation, the third to cancer induced by inflammation. All three conditions were analyzed using three replicates.
2015-06-17 | E-GEOD-57527 | biostudies-arrayexpress
Project description:We examined how prenatal inflammation shapes tissue function and immunity in the lung by reprogramming tissue-resident immune cells from early development. Maternal, but not fetal, type I interferon-mediated inflammation provoked expansion and hyperactivation of group 2 innate lymphoid cells (ILC2s) seeding the developing lung. Hyperactivated ILC2s produced increased IL-5 and IL-13, were associated with acute Th2 bias, decreased Tregs, and persistent lung eosinophilia into adulthood. ILC2 hyperactivation was recapitulated by adoptive transfer of a fetal liver precursor following prenatal inflammation, indicative of developmental programming at the fetal progenitor level. Reprogrammed ILC2 hyperactivation and subsequent lung immune remodeling, including persistent eosinophilia, was associated with worsened histopathology and increased airway dysfunction equivalent to papain exposure, indicating increased asthma susceptibility in offspring. Our data elucidate a potential mechanism by which early-life inflammation results in increased asthma susceptibility, driven by hyperactivated ILC2s that drive persistent changes to lung immunity during perinatal development.
2024-06-24 | GSE268129 | GEO
Project description:OGR1 is a pH sensing G protein-coupled receptor involved in intestinal homeostasis and inflammation. Up-regulation of genes, mediated by OGR1, in response to extracellular acidification were enriched for inflammation, immune response, actin cytoskeleton and cell adhesion pathways. Microarray profiling was performed to compare global gene expression of Ogr1 KO and WT residential peritoneal macrophages in response to an acidic pH shift (pH 6.7, 24 h)
2015-04-12 | E-GEOD-60295 | biostudies-arrayexpress
Project description:Death of intestinal epithelial cells (IECs) is important in the pathological process of intestinal inflammatory diseases. TNF acts as one pathogenic driver for inducing IEC death and substantial intestinal inflammation. However, the physiological protective mechanisms for suppressing TNF-induced IEC death remain poorly understood. Here, we report that EF-hand domain-containing protein D2 (EFHD2), highly expressed in normal intestine tissues but decreased in intestinal biopsy samples of ulcerative colitis patients, protects the intestinal epithelium from TNF-induced IEC apoptosis. EFHD2 inhibits TNF-induced apoptosis in primary IECs and intestinal organoids (enteroids). Mice deficient of Efhd2 in IECs exhibit excessive IEC death and exacerbated experimental colitis. Mechanistically, EFHD2 interacts with Cofilin to suppress the phosphorylation of Cofilin, leading to the inhibition of TNF receptor Ⅰ (TNFR1) internalization and TNF-induced apoptosis. Our findings define EFHD2 as an endogenous suppressor of IEC death to protect intestine inflammation, providing new insight to the regulation of death receptor signaling and control of intestinal inflammatory diseases.
2024-01-14 | PXD048587 |
Project description:The goal of this project is to investigate the role of glucocorticoids and their receptor, glucocorticoid receptor (GR), in intestinal stress response and tissue homeostasis. Using a mouse model with specific deletion of GR in intestinal epithelium (GR iKO mice), we recently discovered that intestinal epithelial GR deficiency deteriorates acute colitis while reducing chronic inflammation-associated colon cancer formation in mice. To understand the molecular mechanisms underlying these phenotypes, we examined colonic transcriptomes of Flox control and GR iKO mice treated with or without dextran sulfate sodium (DSS) for 7 days by microarray analysis.
2021-11-15 | GSE146048 | GEO
Project description:Intestinal inflammation in Atlantic salmon was studied by profiling the intestine mucus proteome, employing isobaric tags for relative and absolute quantification and 2D LC-MS/MS approach. Two fish groups were fed soy saponin-containing (inflammation inducer, SO) or devoid (CO) diets for 36 days. Two more fish groups were fed each of the aforementioned diets with a health additive (CP, SP). Inflammation characteristics in the intestine were milder in the SP-fed fish compared to the SO-fed fish, based on histology results. The fish that had intestinal inflammation (SO) was characterised by alterations of many proteins. Based on the enriched KEGG pathways and GO terms of the SO vs CO comparison pathways such as phagosome and lipid binding were affected due to upregulation of protein like Integrin beta 2 precursor, Coronin 1A, Cathepsin S precursor, Vesicle-trafficking protein, and Neutrophil cytosol factors. On the other hand, the SP group had fewer inflammation characteristics and altered proteins; this fish group had higher abundance of protein linked to the pathways aminoacyl-tRNA biosynthesis and ribosome due to the higher abundance of many large and small subunit of ribosomes. The alteration of Glycogen phosphorylase and Glutamin synthetase could also have alleviated intestinal inflammation in the SP group. Elevating the abundance of ribosomal proteins, aminoacyl-tRNA ligases, and lowering the abundance of Glycogen phosphorylase and Glutamine synthetase could be effective to alleviate intestinal inflammation. The proteins described here can be exploited to alleviate intestinal inflammation in fish and higher vertebrates.
2022-02-14 | PXD029849 | Pride
Project description:Background: Although a number of intestinal inflammatory conditions pertain to the ileum, whole-genome gene expression analyses on ileal inflammation in animal models are lacking to date. Therefore, we aimed to identify and characterize alterations in gene expression in the acutely inflamed ileum of two murine models of intestinal inflammation, namely intestinal schistosomiasis and TNBS-induced ileitis, using Agilent whole-genome microarrays followed by bioinformatics analysis to detect enrichment of Kyoto Encyclopedia of Genes and Genomes pathways and Gene Ontology categories. Results: When compared with healthy control mice, of almost all known mouse genes and transcripts represented on the array, intestinal schistosomiasis and TNBS-induced ileitis yielded 207 and 1417 differential genes respectively, with 48 overlapping genes (adj.p.value<0.1 and log2FC>1 or <1). Complement and coagulation cascades, extracellular matrix-receptor interaction, Fc epsilon receptor I signaling pathways and protein activation cascade, cell adhesion categories were enriched for differential genes in intestinal schistosomiasis. Antigen processing and presentation, cell adhesion molecules, ABC transporters, Toll-like receptor signaling pathways and response to chemical stimulus categories were enriched for differential genes in TNBS-induced ileitis. Although cytokine-cytokine receptor interaction, intestinal immune network for immunoglobulin A production, focal adhesion pathways and immune, inflammatory and defense response categories were enriched for differential genes in both inflammation models, the vast majority of the associated differential genes were unique to each model. Conclusions: This study characterized the two diverse models of ileal inflammation at a whole-genome level and outlined their underlying molecular heterogeneity. The results indicate that intestinal schistosomiasis involves Th2 responses, enhanced tissue repair and complement activation, while TNBS-induced ileitis involves Th17 responses, defective antigen processing and presentation and altered Toll-like receptor-mediated responses. Epithelial barrier impairment seems to occur in both inflammation models. Moreover, the comprehensive differential gene-list provided by this study would be helpful as a starting point to explore a specific novel pathway in more detail dealing with small bowel inflammation. A total of 9 biological samples containing 3 each of Control, S.mansoni-infected and TNBS-treated were included in the study. A reference design was used including a reference sample containing a pool of equimolar amounts of all Control samples. The design consisted totally of 11 arrays which included 3 biological replicates each of Control (labeled in Cy5), S.mansoni-infected (labeled in Cy3) and TNBS-treated tissue samples(labeled in Cy5) as well as two dye flipped technical replicates of a Control and a S.mansoni-infected tissue sample. The reference was labeled with either Cy5 or Cy3, depending on the labeling of the test sample.
2012-10-05 | E-GEOD-31265 | biostudies-arrayexpress