Unidentified
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB19249 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR670144_1.fastq.gz | Fastqsanger.gz | |||
| DRR670144_2.fastq.gz | Fastqsanger.gz | |||
| DRR670145_1.fastq.gz | Fastqsanger.gz | |||
| DRR670145_2.fastq.gz | Fastqsanger.gz | |||
| DRR670146_1.fastq.gz | Fastqsanger.gz |
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Project description:Host-pathogen interactions, in particular during the early stage of infection, are important for the fate of boththe invading pathogen and host. In pathogens, these interactions activate diverse pahogenic signals to cause disease in the host and evade the inevitably activated immune responses of the infected host. In this study, we used in vitro assay system and RNA-seq to analyze the time-resolved genome-wide gene expressions of Xoo evoked by the interactions with rice leaf extracts. RNA-seq analysis was carried out with samples of 3 different time points within 2 hours
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Project description:Host-pathogen interactions involve two critical strategies: resistance, whereby hosts clear invading microbes, and tolerance, whereby hosts carry high pathogen burden asymptomatically. Here, we investigate mechanisms by which Salmonella- superspreader hosts (SSP) maintain an asymptomatic state during chronic infection. We found that regulatory T cells (Tregs) are essential for this disease-tolerant state, limiting intestinal immunopathology and enabling SSP hosts to thrive, while facilitating Salmonella transmission. Treg depletion in SSP mice resulted in decreased survival, heightened gut inflammation and impairment of the intestinal barrier, without affecting Salmonella persistence. Colonic Tregs from SSP mice exhibited a unique transcriptomic profile characterized by the upregulation type-1 inflammatory genes, including the transcription factor T-bet. In the absence of Tregs, we observed robust expansion of cytotoxic CD4+ T cells, with CD4+ T cell depletion restoring homeostasis. These results uncover a critical host strategy to establish disease tolerance during chronic enteric infection, providing novel insights into mucosal responses to persistent pathogens and chronic intestinal inflammation.
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