Asthma is a complex, chronic respiratory disease with marked clinical and pathophysiological heterogeneity. Distinct inflammatory phenotypes of eosinophilic, mixed, neutrophilic and paucigranulocytic asthma are identified in patients, but most in vivo mouse models, studying asthma mechanisms, mimic only eosinophilic phenotype in humans. The detailed unbiased in vivo studies on molecular responses among different kinds of inflammation in asthma models are lacking. Therefore, we developed mouse models representing three different inflammatory phenotypes of airway inflammation, namely eosinophilic, mixed, and neutrophilic asthma via different methods of house dust mite sensitisation.
Tight junction, mucin, and inflammasome-related molecules are differentially expressed in eosinophilic, mixed, and neutrophilic experimental asthma in mice.
Specimen part
View SamplesBalanced immune responses in airways of patients with asthma are crucial to succesful clearance of viral infection and proper asthma control.
Rhinovirus-induced epithelial RIG-I inflammasome suppresses antiviral immunity and promotes inflammation in asthma and COVID-19.
Subject, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Reprogramming capacity of Nanog is functionally conserved in vertebrates and resides in a unique homeodomain.
Specimen part
View SamplesNanog null neural stem (NS) cells were reprogrammed to naive pluripotency in 2i/LIF conditions with mouse (m) Nanog and human (h) Nanog. Global gene expression in resulting iPS cells was compared to embryonic stem (ES) cells and nanog null NS cells.
Reprogramming capacity of Nanog is functionally conserved in vertebrates and resides in a unique homeodomain.
Specimen part
View SamplesNanog null neural stem (NS) cells were reprogrammed to naive pluripotency in 2i/LIF conditions with chick (c) and zebrafish (z) Nanog orthologs. Global gene expression was compared to iPS cells derived with mouse (m) Nanog.
Reprogramming capacity of Nanog is functionally conserved in vertebrates and resides in a unique homeodomain.
Specimen part
View SamplesIn order to identify candidate target genes of the OBP1 (At3g50410) transcription factor we used dexamethasone inducible system (Lloyd et al, 1994). A single inducible over-expression line was compared to an empty vector control line 10h after DEX induction to identify candidate genes that were confirmed by quantitative RT-PCR.
The DOF transcription factor OBP1 is involved in cell cycle regulation in Arabidopsis thaliana.
Specimen part
View SamplesThe foregut definitive endoderm is the precursor of many tissues including the liver, pancreas, thyroid, lungs, trachea and oesophagus. However, networks and pathways involved in the early development of the definitive endoderm of mammals are not well studied. To identify genes with potential roles in the early development of the foregut definitive endoderm in mouse embryos, we performed microarray analysis to compare the gene expression profile of foregut endoderm and non-endodermal tissues from early somite-stage mouse embryos.
Rhou maintains the epithelial architecture and facilitates differentiation of the foregut endoderm.
Specimen part
View SamplesResiquimod is a nucleoside analog belonging to the imidazoquinoline family of compounds which is known to signal through Toll-like receptor 7. Resiquimod treatment has been demonstrated to inhibit the development of allergen induced asthma in experimental models. Despite this demonstrated effectiveness, little is known about the molecular events responsible for this effect. The aim of the present study was to elucidate the molecular processes which were altered following resiquimod treatment and antigen challenge in a mouse model of allergic asthma. Employing microarray analysis, we have characterized the asthmatic transcriptome of the murine lung and determined that it includes genes involved in: the control of cell cycle progression, airway remodelling, the complement and coagulation cascades, and chemokine signalling. We have demonstrated that systemic resiquimod administration resulted in the recruitment of NK cells to the lungs of the mice, although no causal relationship between NK cell recruitment and treatment efficacy was found. Furthermore, results of our studies demonstrated that resiquimod treatment resulted in the normalization of the expression of genes involved with airway remodelling and chemokine signalling, and in the modulation of the expression of genes including cytokines and chemokines, adhesion molecules, and B-cell related genes, involved in several aspects of immune function and antigen presentation. Overall, our findings identified several genes, important in the development of asthma pathology, that were normalized following resiquimod treatment thus improving our understanding of the molecular consequences of resiquimod treatment in the lung milieu.
Modulation of the allergic asthma transcriptome following resiquimod treatment.
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View SamplesThe aim of this experiment was to investigate the regulation of gene expression by KLF3 and KLF8 in fetal erythroid cells by analyzing single and double mutant mouse models.
Generation of mice deficient in both KLF3/BKLF and KLF8 reveals a genetic interaction and a role for these factors in embryonic globin gene silencing.
Specimen part
View SamplesThe BcA86 strain is a unique recombinant congenic strain created from parental strains A/J and C57BL/6J. Naive mice from the BcA86 strain have a lung responsiveness phenotype resembling mice from airway hyperresponsive strain A/J. However, majority of the BcA86 genome is from the hyporesponsive strain C57BL/6J. Our goal was to identify the genomic regions that are associated with this BcA86 phenotype. Using F2 mice generated from BcA86 backcrossed to C57BL/6J, we identified a QTL for airway hyperresponsiveness on mouse chromosome 12. We validated the importance of mouse chromosome 12 in airway responsiveness using a chromosome 12 substitution strain (CSS12) which contains A/J chromosome 12 on a C57BL/6J background. The CSS12 strain also had a lung responsiveness phenotype similar to A/J. We selected genes within our QTL as candidates for airway hyperresponsiveness if they contained a deleterious coding variant (based on PROVEAN analysis) or if they were differently expressed between hyperresponsive (A/J, BcA86, CSS12) and hyporesponsive (C57BL/6J) strains.
Mapping of a chromosome 12 region associated with airway hyperresponsiveness in a recombinant congenic mouse strain and selection of potential candidate genes by expression and sequence variation analyses.
Specimen part
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