Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA407446 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6040950_1.fastq.gz | Fastqsanger.gz | |||
| SRR6040950_2.fastq.gz | Fastqsanger.gz | |||
| SRR6040960_1.fastq.gz | Fastqsanger.gz | |||
| SRR6040960_2.fastq.gz | Fastqsanger.gz | |||
| SRR6040951_1.fastq.gz | Fastqsanger.gz |
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Project description:ILC1 confer early host protection at initial sites of viral infection [ATAC-Seq]
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Project description:ILC1 confer early host protection at initial sites of viral infection
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Project description:Innate and adaptive immune cells can acquire “memory” of encounters with a diverse range of activating signals to tune their response to secondary stimuli. Group 1 innate lymphoid cells (ILC1) are recently discovered tissue-resident sentinels that are essential for early host protection from intracellular pathogens at initial sites of infection. However, whether ILC1 function as short-lived effectors or persist and refine their responsiveness following pathogen challenge is not well understood. Furthermore, whether pathogen-derived antigens directly modulate tissue-resident ILC responses remains unclear. Here, we found that liver-resident ILC1 expand locally and persist following the resolution of mouse cytomegalovirus (MCMV) infection. MCMVexperienced ILC1 acquired stable transcriptional, epigenetic, and phenotypic changes, with an enhanced protective effector response to secondary MCMV challenge. Protective memory ILC1 responses were dependent on the MCMV-encoded glycoprotein m12, but not formed during bystander cytokine activation following heterologous infection. Thus, liver ILC1 acquire adaptive features in a MCMV-specific manner.
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Project description:Influenza and other respiratory viral pathogens are leading causes of mortality and morbidity. We previously demonstrated that circadian rhythms confer temporal protection from influenza infection. Here, we investigated whether this protection requires rhythmic function after the initial infection by manipulating environmental cycles. We demonstrate that disrupting environmental lighting cues within a critical window of vulnerability abrogates time-of-day specific protection. This poor outcome is mediated by a dysregulated immune response, evidenced by the accumulation of inflammatory monocytes and CD8+ cells in the lungs and a transcriptomic profile indicative of an exaggerated immune response. Disruption of the light cycle does not affect outcomes in a clock mutant, indicating that it acts by compromising endogenous timekeeping. Importantly, rhythmic meal timing mitigates the adverse effects of disrupted light cycles, suggesting that external cycling cues, which act through different body clocks, can substitute for each other. Our findings highlight the crucial interplay between environmental factors and endogenous clocks in shaping influenza outcomes, offering significant translational potential for improving the care of critically ill patients with respiratory viral infections.
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Project description:This ordinary differential equation model is described in the following article:
"Autocrine and paracrine interferon signalling as ‘ring vaccination’ and ‘contact tracing’ strategies to suppress virus infection in a host"
G. Michael Lavigne, Hayley Russell, Barbara Sherry and Ruian Ke
DOI: 10.1098/rspb.2020.3002
Comment:
This model is based on the ordinary differential equations of the non-spatial model of well-mixed viral infection stated in the manuscript (Eq. 2.1 in the article).
Abstract:
The innate immune response, particularly the interferon response, represents a first line of defence against viral infections. The interferon molecules produced from infected cells act through autocrine and paracrine signalling to turn host cells into an antiviral state. Although the molecular mechanisms of IFN signalling have been well characterized, how the interferon response collectively contribute to the regulation of host cells to stop or suppress viral infection during early infection remain unclear. Here, we use mathematical models to delineate the roles of the autocrine and the paracrine signalling, and show that their impacts on viral spread are dependent on how infection proceeds. In particular, we found that when infection is well-mixed, the paracrine signalling is not as effective; by contrast, when infection spreads in a spatial manner, a likely scenario during initial infection in tissue, the paracrine signalling can impede the spread of infection by decreasing the number of susceptible cells close to the site of infection. Furthermore, we argue that the interferon response can be seen as a parallel to population-level epidemic prevention strategies such as ‘contact tracing’ or ‘ring vaccination’. Thus, our results here may have implications for the outbreak control at the population scale more broadly.
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Project description:we identify gene expression patterns associated with three distinct phases (Infiltrating, Early Inflammatory, Late Inflammatory) in the influenza A virus response of recruited alveolar macrophages. In the Early Inflammatory phase, recruited macrophages begin expressing pro-inflammatory genes, driving cytokine-mediated lung damage and contributing to the morbidity observed in influenza-infected wild-type mice. In mice lacking vimentin (Vim-/-), genes associated with the Early Inflammatory phase are suppressed, while the expression of the Infiltrating Phase genes is maintained, which is associated with protection from influenza-induced injury. Using a bone-marrow chimera mouse model, we validate that Vim-/- recruited alveolar macrophages are sufficient to confer protection from influenza-induced mortality. Our results define the temporal dynamics of gene expression in recruited alveolar macrophages, which shape the host response to infection with respiratory viruses.
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