CME_UFRJ
Ontology highlight
ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR034194.fastq.gz | Fastqsanger.gz | |||
| ERR034195.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 2 of 2 |
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Project description:Atherosclerosis is a disease of mid-to-large arteries characterized by lipid accumulation, chronic inflammation, and pathologic remodeling of the vessel wall. Rupture of atherosclerotic plaques can generate thrombi that occlude blood flow and cause acute myocardial infarction (AMI) and acute ischemic stroke (AIS) that are leading causes of death and disability. Patients that develop severe bacterial infections are at increased risk of AMI and AIS, but the mechanisms underlying this association have not been well-characterized. Previous studies have reported that low-density lipoprotein (LDL) carries bacterial small (s)RNAs that can influence macrophage polarization within plaques, but whether infection alters LDL-associated sRNA or atherosclerotic plaque characteristics to promote AMI/AIS is unclear. Here, we tested whether chronic infection by the Gram-positive pathobiont Staphylococcus aureus was sufficient to alter LDL-associated bacterial sRNA and promote pathogenic changes in atheromatous plaques. Using a mouse model of injury-associated S. aureus osteomyelitis, we report minimal changes in the bacterial sRNA composition of LDL with no obvious changes in pathogen-derived sRNA on LDL of either normolipidemic or hyperlipidemic mice. Unexpectedly, hyperlipidemic mice with chronic osteomyelitis showed a reduction in plaque area within the aortic root relative to sham mice. Although these results do not explain increased risk of AMI/AIS in patients, we observed that hyperlipidemic mice had reduced bacterial burden and reduced bone disease relative to normolipidemic mice infected with S. aureus. Together, these findings highlight unresolved questions regarding the origin of bacterial sRNA associated with LDL and suggests that hyperlipidemia contributes to host protection against invasive S. aureus infection.
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Project description:Transcriptional profiling of mouse embryonic stem cells comparing Mutant PDL cells and healthy PDL cells to study Radiculomegaly (excessive dental root elongation) Two-condition experiment, Mutant vs. Healthy PDL cells, technological triplicate
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Project description:Bacterial genotoxins, produced by several Gram-negative bacteria, induce DNA damage in the target cells. While the responses induced in the host cells have been extensively studied in vitro, the role of the genotoxins as effectors during the course of acute and chronic infections remains poorly characterized.To address this issue, we assessed the effects of the Salmonella enterica genotoxin, known as typhoid toxin, in in vivo models of murine chronic infections. Immunocompetent mice were chronically infected with isogenic S. enterica, serovar Typhimurium (S. Typhimurium) strains, encoding either a functional (MC71-TT) or an inactive (MC71-DcdtB) typhoid toxin. Keywords: salmonella typhimurium, bacterial genotoxins, typhoid toxin, chronic infection, mice model
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Project description:Chronic apical periodontitis, typified by inflammatory granulation tissue formation and alveolar bone destruction, is the immune response around the apical root caused by long-term infection and pathogenic stimulation in the root canal. Through the recruitment and infiltration of immune cells and inflammatory mediators, wound healing begins accompanied by the starting of infection. Hence, a comprehensive understanding of biological processes and disease development from the cellular microenvironment in inflammatory periapical areas has important implications.
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Project description:Bacterial genotoxins, produced by several Gram-negative bacteria, induce DNA damage in the target cells. While the responses induced in the host cells have been extensively studied in vitro, the role of the genotoxins as effectors during the course of acute and chronic infections remains poorly characterized.To address this issue, we assessed the effects of the Salmonella enterica genotoxin, known as typhoid toxin, in in vivo models of murine chronic infections. Immunocompetent mice were chronically infected with isogenic S. enterica, serovar Typhimurium (S. Typhimurium) strains, encoding either a functional (MC71-TT) or an inactive (MC71-DcdtB) typhoid toxin. Keywords: salmonella typhimurium, bacterial genotoxins, typhoid toxin, chronic infection, mice model Transcriptomic analysis was performed on intestine tissues (colon, jejunum and ileum) and liver collected from 129S6/SvEvTac mice, either uninfected or infected with S. typhimurium MC71 strains (strain MC71-TT, expressing a functional typhoid toxin, and strain MC71-dcdtB, expressing an inactive typhoid toxin) for 60 days
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Project description:Understanding the response of memory CD8 T cells to persistent antigen re-stimulation and the role of CD4 T cell help is critical to the design of successful vaccines for chronic diseases. However, studies comparing the protective abilities and qualities of memory and naïve cells have been mostly performed in acute infections, and little is known about their roles during chronic infections. Herein, we show that memory cells dominate over naïve cells and are protective when present in large enough numbers to quickly reduce infection. In contrast, when infection is not rapidly reduced, memory cells are quickly lost, unlike naïve cells. This loss of memory cells is due to (i) an early block in cell proliferation, (ii) selective regulation by the inhibitory receptor 2B4, and (iii) increased reliance on CD4 T cell help. These findings have important implications towards the design of T cell vaccines against chronic infections and tumors. 16 samples are analyzed: 3 replicates of secondary effector CD8 P14 T cells at day 8 post-acute lymphocytic choriomeningitis virus (LCMV) infection; 4 replicates of secondary effector CD8 P14 T cells at day 8 post-chronic LCMV infection; 4 replicates of primary effector CD8 P14 T cells at day 8 post-acute LCMV infection; and 5 replicates of primary effector CD8 P14 T cells at day 8 post-chronic LCMV infection.
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