Zebrafish il-4 il-10 regulated immunity in gills
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ABSTRACT:
PROVIDER: PRJEB37851 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4029240_1.fastq.gz | Fastqsanger.gz | |||
| ERR4029240_2.fastq.gz | Fastqsanger.gz | |||
| ERR4029250_1.fastq.gz | Fastqsanger.gz | |||
| ERR4029250_2.fastq.gz | Fastqsanger.gz | |||
| ERR4029241_1.fastq.gz | Fastqsanger.gz |
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Project description:Zebrafish il-4 il-10 regulated immunity in gills
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Project description:Host immunity limits iron availability to pathogenic bacteria, but whether immunity limits pathogenic bacteria from accessing host heme, the major source of iron in the body, remains unclear. Using Citrobacter rodentium, a mouse enteric pathogen and Escherichia coli, a major cause of sepsis in humans as models, we find that interleukin-22, a cytokine best known for its ability to promote epithelial barrier function, also suppresses the systemic growth of bacteria by limiting iron availability to the pathogen. Using an unbiased proteomic approach to understand the mechanistic basis of IL-22 dependent iron retention in the host, we have identified that IL-22 induces the production of the plasma hemoglobin scavenger haptoglobin and heme scavenger hemopexin. Moreover, the anti-microbial effect of IL-22 depends on the induction of hemopexin expression, while haptogloblin is dispensable. Impaired pathogen clearance in infected Il22-/- mice was restored by hemopexin administration and hemopexin-deficient mice had increased pathogen loads after infection. These studies reveal a previously unrecognized host defense mechanism regulated by IL-22 that relies on the induction of hemopexin to limit heme availability to bacteria leading to suppression of bacterial growth during systemic infections.
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Project description:More and more evidence prove that deltamethrin (Del) exposure induced the adverse effect and damaged immune function to the aquatic animals in the parasite killing process with increasing insecticide application. However, little is currently known of the negative effect on mucosal immunity, especially in gills tissue. In this study, the LC50 of deltamethrin on gibel carp at 96h was determined to be 6.194 μg/L, and then juvenile gibel carp (Carassius auratus gibelio) (8.8 ± 1.0 g) were exposed to four Del exposure groups (0.61, 1.22, 2.44, and 4.88 μg/L) for 12h and 24h. To evaluate the innate immune-related enzymes in gills tissue, we measured the lysozyme (LYZ) and myeloperoxidase (MPO) contents and found that with increased concentration of Del exposure, the LYZ content was found to increase in the 1.22 μg/L Del group initially significantly and then gradually significantly decrease in the 4.88 μg/L Del group. And the activity of MPO was significantly lifted in a dose-dependent manner. The histological analysis showed that Del exposure serious desquamation and necrosis in the surface of epithelial cells are often found, accompanied by interlamellar cellular mass degenerative. In addition, the mucous cells were significantly decreased in the high Del concentration group (2.44 μg/L and 4.88 μg/L Del group) by AB-PAS staining. Importantly, totally 2857 DEGs (including 1624 up-regulated and 1233 down-regulated genes) were identified in the gill between the control group and 4.88μg/L Del exposure group using comparative transcriptional analysis. Among these, some genes involved in innate immune molecules, complement activation, apoptosis-related molecules, cytokine, and adaptive immune molecules, were also down-regulated. Importantly, we found several signal pathways related to immune response were downregulated, such as immune system process and tumor necrosis factor receptor (superfamily) binding pathways based on the GO and KEGG enrichment analysis. Consistently, we detect the expression of pro-inflammatory cytokines (TNF-α, IFN-γ, IL-1β, and IL-8), anti-inflammatory cytokines (TGF-β), LYZ, IgM, and Hsp70 in the gills tissue at 12h and 24h after Del exposure, which were consistent with our sequencing results. Collectively, these results demonstrated that the gills mucosa injury and immunotoxicity was induced by Del exposure and provided novel insight for explaining to some extent why Del-exposure fish and are more susceptible to concurrent or secondary viral or bacterial infections.
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