Ontology highlight
ABSTRACT:
PROVIDER: PRJNA419072 | ENA |
REPOSITORIES: ENA
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Project description:Background: The role of host encoded microRNAs in genetically determined host susceptibility to influenza A virus (IAV) infection has not been explored. We therefore compared changes in pulmonary miRNA expression during IAV infection in two inbred mouse strains with differential susceptibility to IAV infection. Results: miRNA expression profiles were determined in lungs of the more susceptible mouse strain DBA/2J and the less susceptible strain C57BL/6J within 120 hours post infection (hpi) with IAV (H1N1) PR8. Even the miRNomes of uninfected lungs differed substantially between the two strains. After a period of relative quiescence, major miRNome reprogramming was detected in both strains by 48 hpi and increased through 120 hpi. Distinct groups of miRNAs regulated by IAV infection could be defined: (1) miRNAs (n= 39) whose expression correlated with HA mRNA expression and represented the general response to IAV infection independent of host genetic background; (2) miRNAs (n=20) whose expression correlated with HA mRNA expression but differed between the two strains; and (3) remarkably, miRNAs (n=8) whose abundance even in uninfected lungs differentiated nearly perfectly (area under the ROC curve >0.99) between the two strains throughout the time course. Higher abundance of miRNAs with anti-apoptotic functions and lower abundance of miRNAs regulating the PI3K-Akt pathway were associated with the more susceptible DBA/2J strain. Conclusions: These results suggest that differences in host miRNA abundance before and during IAV infection are in part determined genetically and contribute to susceptibility to IAV infection in this experimental mouse model, and likely in humans.
2017-06-12 | GSE89064 | GEO
Project description:Previous studies have documented the diversity of genetic background of methicillin-resistant S. aureus (MRSA) strains associated with healthcare (HA-MRSA), community (CA-MRSA) and livestock (LA-MRSA). The accessory and core-variable genome content of those strains remain largely unknown. To compare the composition of accessory and core-variable genome of Belgian MRSA strains according to host, population setting and genetic background, representative strains of HA- (n=21), CA- (n = 13) and ST398 LA-MRSA (n = 18) were characterized by a DNA-microarray (StaphVar Array) composed of oligonucleotide probes targeting ~400 resistance, adhesion and virulence associated genes.ST398 strains displayed very homogenous hybridization profiles (>94% gene content homology) irrespective of their host origin. This “ST398-specific” genomic profile was not distantly demarked from those of certain human-associated lineages but lacked several virulence- and colonization-associated genes harbored by strains of human origin, such as genes encoding proteases, haemolysins or adhesins. No enterotoxin gene was found among ST398 strains. In conclusion, our findings are consistent with a non-human origin of this ST398 lineage but suggest that it might have the potential to adapt further to the human host.
2010-11-15 | GSE20541 | GEO
Project description:Aim of this project is to identify biomarkers associated with persistance of Candida strains in the host and with virulence/pathogenicity of the different strains
2016-04-30 | E-SYBR-9 | biostudies-arrayexpress
Project description:This model simulates the colonization of the mouse gut with different strains of Yersinia enterocolitica. Thereby it takes the host-immune repsone into account. The parameters are calibrated based on experimentally obtained data (faces of different mice).
2022-02-16 | MODEL2002070001 | BioModels
Project description:Aim of this project is to identify biomarkers associated with fungal persistence in the host and genomic variability among strains isolated from different environments.
2016-04-30 | E-SYBR-8 | biostudies-arrayexpress
Project description:Gene expression changes in the lung was studied by RNAseq in different CC mouse strains infected with influenza A virus. Results: Strong differences between the genetically CC mouse strains can be observed in the activation of host defense genes. These differences can be related to genetic variants in the genome of the CC strains. Furthermore, different strains exhibit variant susceptibility to infections (body weight loss and survival). These differences can be correlated to differences in gene expression profiles.
2020-07-08 | GSE136748 | GEO
Project description:Draft genome sequences of 12 host-associated Lactobacillus reuteri strains
| PRJNA587310 | ENA
Project description:Seasonal influenza outbreaks and recurrent influenza pandemics present major challenges to public health. By studying immunological responses to influenza in different host species, it may be possible to discover common mechanisms of susceptibility in response to various influenza strains. This could lead to novel therapeutic targets with wide clinical application. Using a mouse-adapted strain of influenza (A/HK/1/68-MA20 [H3N2]), we produced a mouse model of severe influenza (p-flu) that reproduces the hallmark high viral load and overexpression of cytokines associated with susceptibility to p-flu in humans. We mapped genetic determinants of the host response using a panel of 29 closely related mouse strains (AcB/BcA panel of recombinant congenic strains) created from influenza-susceptible A/J and influenza-resistant C57BL/6J (B6) mice. Combined clinical quantitative trait loci (cQTL) and lung expression QTL (eQTL) mapping identified candidate genes for two sex-specific QTLs on chromosomes 2 and 17. The former includes the previously described Hc gene, a deficit of which is associated with the susceptibility phenotype in females. The latter includes the phospholipase gene Pla2g7 and Tnfrsf21, a member of the tumor necrosis factor receptor superfamily. Confirmation of the gene underlying the chromosome 17 QTL may reveal new strategies for influenza treatment.
2012-05-02 | GSE35888 | GEO
Project description:The pathological outcomes of schistosomiasis are largely dependent on the molecular and cellular mechanisms of the host immune response. In this study, we demonstrate the variation of host gene expression which underlies the contrasting hepatic pathology observed between two inbred mouse strains following schistosome infection. Whole genome microarray analysis was employed in conjunction with histological and immunohistochemical analysis to define and compare the hepatic gene expression profiles and cellular composition associated with the hepatopathology observed in BALB/c and CBA mice during an active Schistosoma japonicum infection. Here, we show that the transcriptional profiles differ significantly between the two mouse strains with high statistical confidence. We identified specific genes correlating with the more severe pathology associated with CBA mice, as well as genes which may confer the milder degree of pathology associated with BALB/c mice. Generally, up-regulated genes were largely associated with immune and inflammatory responses, antigen processing and cytokine/chemokine activity. In BALB/c mice, neutrophil genes exhibited striking increases in expression, which coincided with significantly greater accumulation of neutrophils at granulomatous regions, compared to CBA mice. In contrast, up-regulated expression of eosinophil chemokine CCL24 in CBA mice paralleled the cellular influx of eosinophils to the hepatic granulomas. Additionally, there was greater down-regulation of genes involved in metabolic processes in CBA mice, reflecting the greater degree of liver damage in these mice. Genes involved in fibrosis showed similar levels of expression in both mouse strains. Genes associated with Th1 and Th2 responses showed no significant differences in expression between strains. These results provide a more complete picture of the molecular and cellular mechanisms which govern the pathological outcome of hepatic schistosomiasis. Furthermore, this improved understanding of schistosome immunopathogenesis in the murine model will provide the basis for a better appreciation of the complexities associated with chronic human schistosomiasis.
2010-11-30 | GSE25713 | GEO