Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA92443 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Airway Epithelial Cell Response to Sendai virus infection
| PRJNA108331 | ENA
Project description:Expression data from BMDC cells with or without Sendai virus infection
| PRJNA147773 | ENA
Project description:Small RNAs were profiled during Sendai virus infection of human A549 cells to identify changes in microRNA abundance during the cellular antiviral response. Examination of microRNA abundance during Sendai virus infection.
2013-06-10 | E-GEOD-43966 | biostudies-arrayexpress
Project description:Early life respiratory viral infections and atopic characteristics are significant risk factors for the development of childhood asthma. It is hypothesized that repeated respiratory viral infections might induce structural remodeling by interfering with the normal process of lung maturation; however, the specific molecular processes that mediate these developments are not understood. To define relevant molecular pathways, we used a well-established Sendai virus infection model in weanling rats to compare transcriptome signatures between a post-infection asthma prone susceptible strain (BN) and a post-infection asthma resistant strain (F344). Specific to this weanling model and not described in adult models, Sendai virus infection in the susceptible strain resulted in morphological abnormalities in distal airways that persist into adulthood, suggesting a disruption of normal lung growth. Gene expression data from infected and control lungs across five time points indicated that specific features of the immune response following viral infection were heightened and prolonged in lungs from BN compared with F344 rats. These features included an increase in macrophage cell number and related gene expression, which then transitioned to an increase in mast cell number and related gene expression. In contrast to the heightened immune response in infected BN lungs, infected F344 lungs displayed more efficient re-epithelialization. We conclude that the structural defects that developed and persisted in infected BN but not F344 lungs were preceded by a pronounced macrophage and mast cell response to viral infection acting in parallel with an inadequate re-epithelialization. For each of the five time points, one array was run for each of the four conditions (F344 control, BN control, F344 virus, BN virus) with 15 individual smaples pooled on each array.
2013-10-01 | E-GEOD-51267 | biostudies-arrayexpress
Project description:Small RNAs were profiled during Sendai virus infection of human A549 cells to identify changes in microRNA abundance during the cellular antiviral response.
2013-06-10 | GSE43966 | GEO
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:Innate immunity is the first line of defense against viral and microbial pathogens. BMDC is critical for innate immunity. To investigate the complicated net signaling after virus invasion, we did a cDNA microarray analysis of BMDC with or without Sendai Virus infection. We used microarrays to find proteins that upregulated by Sendai Virus infection and investigated if these proteins had functions in regulating Sendai Virus induced signaling pathway. BMDC cells are seperated from C57BL6 mice, infected with Sendai Virus or not,cultured and harveseted for RNA extraction and hybridization on Affymetrix microarrays
2011-12-08 | E-GEOD-32499 | biostudies-arrayexpress
Project description:Innate immunity is the first line of defense against viral and microbial pathogens. BMDC is critical for innate immunity. To investigate the complicated net signaling after virus invasion, we did a cDNA microarray analysis of BMDC with or without Sendai Virus infection. We used microarrays to find proteins that upregulated by Sendai Virus infection and investigated if these proteins had functions in regulating Sendai Virus induced signaling pathway.
2011-12-08 | GSE32499 | GEO
Project description:Airway Epithelial Cell Response to Sendai virus infection
2014-07-03 | E-GEOD-10211 | ExpressionAtlas
Project description:Early life respiratory viral infections and atopic characteristics are significant risk factors for the development of childhood asthma. It is hypothesized that repeated respiratory viral infections might induce structural remodeling by interfering with the normal process of lung maturation; however, the specific molecular processes that mediate these developments are not understood. To define relevant molecular pathways, we used a well-established Sendai virus infection model in weanling rats to compare transcriptome signatures between a post-infection asthma prone susceptible strain (BN) and a post-infection asthma resistant strain (F344). Specific to this weanling model and not described in adult models, Sendai virus infection in the susceptible strain resulted in morphological abnormalities in distal airways that persist into adulthood, suggesting a disruption of normal lung growth. Gene expression data from infected and control lungs across five time points indicated that specific features of the immune response following viral infection were heightened and prolonged in lungs from BN compared with F344 rats. These features included an increase in macrophage cell number and related gene expression, which then transitioned to an increase in mast cell number and related gene expression. In contrast to the heightened immune response in infected BN lungs, infected F344 lungs displayed more efficient re-epithelialization. We conclude that the structural defects that developed and persisted in infected BN but not F344 lungs were preceded by a pronounced macrophage and mast cell response to viral infection acting in parallel with an inadequate re-epithelialization.
2013-10-01 | GSE51267 | GEO