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.
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.
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.
Project description:Introgressed variants from other species can be an important source of genetic variation because they may arise rapidly, can include multiple mutations on a single haplotype, and have often been pretested by selection in the species of origin. Although introgressed alleles are generally deleterious, several studies have reported introgression as the source of adaptive alleles-including the rodenticide-resistant variant of Vkorc1 that introgressed from Mus spretus into European populations of Mus musculus domesticus. Here, we conducted bidirectional genome scans to characterize introgressed regions into one wild population of M. spretus from Spain and three wild populations of M. m. domesticus from France, Germany, and Iran. Despite the fact that these species show considerable intrinsic postzygotic reproductive isolation, introgression was observed in all individuals, including in the M. musculus reference genome (GRCm38). Mus spretus individuals had a greater proportion of introgression compared with M. m. domesticus, and within M. m. domesticus, the proportion of introgression decreased with geographic distance from the area of sympatry. Introgression was observed on all autosomes for both species, but not on the X-chromosome in M. m. domesticus, consistent with known X-linked hybrid sterility and inviability genes that have been mapped to the M. spretus X-chromosome. Tract lengths were generally short with a few outliers of up to 2.7 Mb. Interestingly, the longest introgressed tracts were in olfactory receptor regions, and introgressed tracts were significantly enriched for olfactory receptor genes in both species, suggesting that introgression may be a source of functional novelty even between species with high barriers to gene flow.
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.
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
Project description:Translational research is commonly performed in the C57B6/J mouse strain, chosen for its genetic homogeneity and phenotypic uniformity. Here, we evaluate the suitability of the white-footed deer mouse (Peromyscus leucopus) as a model organism for aging research, offering a comparative analysis against C57B6/J and diversity outbred (DO) Mus musculus strains. Our study includes comparisons of body composition, skeletal muscle function, and cardiovascular parameters, shedding light on potential applications and limitations of P. leucopus in aging studies. Notably, P. leucopus exhibits distinct body composition characteristics, emphasizing reduced muscle force exertion and a unique metabolism, particularly in fat mass. Cardiovascular assessments showed changes in arterial stiffness, challenging conventional assumptions and highlighting the need for a nuanced interpretation of aging-related phenotypes. Our study also highlights inherent challenges associated with maintaining and phenotyping P. leucopus cohorts. Behavioral considerations, including anxiety-induced responses during handling and phenotyping assessment, pose obstacles in acquiring meaningful data. Moreover, the unique anatomy of P. leucopus necessitates careful adaptation of protocols designed for Mus musculus. While showcasing potential benefits, further extensive analyses across broader age ranges and larger cohorts are necessary to establish the reliability of P. leucopus as a robust and translatable model for aging studies.
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.