Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1222585 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32860426_1.fastq.gz | Fastqsanger.gz | |||
| SRR32860427_1.fastq.gz | Fastqsanger.gz | |||
| SRR32860427_2.fastq.gz | Fastqsanger.gz | |||
| SRR32860428_1.fastq.gz | Fastqsanger.gz | |||
| SRR32860429_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
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Project description:Staphylococcus aureus (S. aureus) is a known pathogen able to infect humans and animals. Human S. aureus isolates are often associated with carriage of Sa3int prophages combined with loss of beta-hemolysin production due to gene disruption, whereas animal isolates are positive for beta-hemolysin associated with absence of Sa3int prophages. Sa3int prophages are known to contribute to staphylococcal fitness and virulence in human host by providing human-specific virulence factors encoded on the prophage genome. Strain-specific differences in regard to phage transfer, lysogenization and induction are attributable to yet unknown staphylococcal factors specifically influencing prophage gene expression. In this work we used tagRNA-sequencing approach to specifically search for these unknown host factors and differences in prophage gene expression. For this purpose, we established a workflow revealing the first direct comparison for differential gene expression analysis on two distinct single-lysogenic S. aureus isolates. Further, global gene expression patterns were investigated in two S. aureus isolates upon mitomycin C treatment and compared to uninduced conditions. This provides new insights into the tightly linked host-phage interaction network.
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Project description:Atopic dermatitis (AD) is a chronic pruritic inflammatory skin disease. We recently described an animal model in which repeated epicutaneous applications of a house dust mite extract and Staphylococcal enterotoxin B induced eczematous skin lesions. In this study we showed that global gene expression patterns are very similar between human AD skin and allergen/staphylococcal enterotoxin B–induced mouse skin lesions, particularly in the expression of genes related to epidermal growth/differentiation, skin barrier, lipid/energy metabolism, immune response, or extracellular matrix. In this model, mast cells and T cells, but not B cells or eosinophils, were shown to be required for the full expression of dermatitis, as revealed by reduced skin inflammation and reduced serum IgE levels in mice lacking mast cells or T cells (TCRb-/- or Rag1-/-). The clinical severity of dermatitis correlated with the numbers of mast cells, but not eosinophils. Consistent with the idea that T helper type 2 (Th2) cells play a predominant role in allergic diseases, the receptor for the Th2-promoting cytokine thymic stromal lymphopoietin and the high-affinity IgE receptor, FceRI, were required to attain maximal clinical scores. Therefore, this clinically relevant model provides mechanistic insights into the pathogenic mechanism of human AD. A total of six samples were analyzed. Back skin samples from healthy or AD-induced C57BL/6, PLC-beta 3 KO (C57BL/6 background), and NC/Nga mice were collected for total RNA extraction. Pooled RNA from 2-4 mice per condition were used for analysis.
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