Very little is known about how animals discriminate pathogens from innocuous microbes. To address this question, we examined infection-response gene induction in the nematode Caenorhabditis elegans. We focused on genes that are induced in C. elegans by infection with the bacterial pathogen Pseudomonas aeruginosa, but are not induced by an isogenic attenuated gacA mutant. Most of these genes are induced independently of known immunity pathways. We generated a GFP reporter for one of these genes, infection response gene 1 (irg-1), which is induced strongly by wild-type P. aeruginosa strain PA14, but not by other C. elegans pathogens or by other wild-type P. aeruginosa strains that are weakly pathogenic to C. elegans. To identify components of the pathway that induces irg-1 in response to infection, we performed an RNA interference screen of C. elegans transcription factors. This screen identified zip-2, a bZIP transcription factor that is required for inducing irg-1, as well as several other genes, and is important for defense against infection by P. aeruginosa. These data indicate that zip-2 is part of a specialized pathogen response pathway that is induced by virulent strains of P. aeruginosa and provides defense against this pathogen.
bZIP transcription factor zip-2 mediates an early response to Pseudomonas aeruginosa infection in Caenorhabditis elegans.
Time
View SamplesAnalysis of differential gene expression in C. elegans adults exposed to three different bacteria: E. coli strain OP50, wild-type P. aeruginosa PA14 and gacA mutant PA14. Samples were analyzed at 4 hours and 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection.
p38 MAPK regulates expression of immune response genes and contributes to longevity in C. elegans.
Specimen part
View SamplesAnalysis of genes differentially expressed between daf-2(e1368) and daf-2(e1368);pmk-1(km25) and between daf-2(e1368) and daf-2(e1368);daf-16(mgDf47). These studies identified genes upregulated by wild-type PMK-1 and wild-type DAF-16.
p38 MAPK regulates expression of immune response genes and contributes to longevity in C. elegans.
Specimen part
View SamplesYoung adult fer-15;fem-1 Caenorhabditis elegans were infected with Staphylococcus aureus for 8 h to determine the transcriptional host response to Staphylococcus aureus. Analysis of differential gene expression in C. elegans young adults exposed to two different bacteria: E. coli strain OP50 (control), wild-type Staphylococcus aureus RN6390. Samples were analyzed at 8 hours after exposure to the different bacteria. These studies identified C. elegans genes induced by pathogen infection.
Distinct pathogenesis and host responses during infection of C. elegans by P. aeruginosa and S. aureus.
Disease, Disease stage
View SamplesThe goal of the study is to identify p53 target genes specific to macrophages using the p53 stabilizer, Nutlin-3.
p53 and NF-κB coregulate proinflammatory gene responses in human macrophages.
Sex, Age, Specimen part, Disease, Treatment, Race, Subject
View SamplesThe samples are a part of a study aiming at diagnosing ulcerative colitis from genome-wide gene expression analysis of the colonic mucosa. Colonic mucosal samples were collected as endoscopic pinch biopsies from ulcerative colitis patients and from control subjects. Samples with and without macroscopic signs of inflammation were collected from the patients.
Diagnosis of ulcerative colitis before onset of inflammation by multivariate modeling of genome-wide gene expression data.
No sample metadata fields
View SamplesIt was the purpose to analyse the changes in gene expression which occur in the mouse small intestine from the pre-weaning to the post-weaning stage. The gene expression was accordingly followed from postnatal day 4 to postnatal day 32.
Cellular cross talk in the small intestinal mucosa: postnatal lymphocytic immigration elicits a specific epithelial transcriptional response.
No sample metadata fields
View SamplesGene expression of mouse hepatic stellate cells was characterized under the following conditions:
Deactivation of hepatic stellate cells during liver fibrosis resolution in mice.
Sex, Specimen part
View SamplesThe epithelial expression of the insulin receptor in the colon is previously reported to correlate with the extent of colonic inflammation. Here, we investigated the effect of inactivating the epithelial insulin receptor in the intestinal tract, in an experimental model of inflammation-induced colorectal cancer. We report increased susceptibility to chemically-induced colitis together with potentiated colonic tumorigenesis in the knockout mice. Furthermore, we show that topically administered insulin in inflamed colons of wildtype mice reduces inflammation-induced weight loss and improves remission in a dose-dependent manner. Mice receiving rectal insulin enemas exhibited lower colitis endoscopic scores and developed significantly fewer and smaller tumors compared with the control group receiving phosphate-buffered saline only. Rectal insulin therapy can potentially be a novel treatment targeting the epithelial layer to enhance mucosal healing in the ulcerated areas. Our findings open up new possibilities for combination treatments to synergize with the existing anti-inflammatory therapies.
Rectal Insulin Instillation Inhibits Inflammation and Tumor Development in Chemically Induced Colitis.
Treatment
View SamplesGenes encoding transcription factors function as hubs in gene regulatory networks because they encode DNA-binding proteins, which bind to promoters that carry their binding sites. In the present work we have studied gene regulatory networks defined by genes with transcripts belonging to different mRNA abundance classes in the small intestinal epithelial cell. The focus is the rewiring that occurs in transcription factor hubs in these networks during the differentiation of the small intestinal epithelial cell while it migrates along the crypt-villus axis and during its development from a fetal endodermal cell to a mature adult villus epithelial cell.
Metabolome, transcriptome, and bioinformatic cis-element analyses point to HNF-4 as a central regulator of gene expression during enterocyte differentiation.
No sample metadata fields
View Samples