Ontology highlight
ABSTRACT:
PROVIDER: PRJNA698550 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13601332.fastq.gz | Fastqsanger.gz | |||
| SRR13601333.fastq.gz | Fastqsanger.gz | |||
| SRR13601334.fastq.gz | Fastqsanger.gz | |||
| SRR13601335.fastq.gz | Fastqsanger.gz | |||
| SRR13601336.fastq.gz | Fastqsanger.gz |
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Project description:IL-17 and IL-17R signaling in the intestinal epithelium regulate the intestinal microbiome. Given the reported links between intestinal dysbiosis, bacterial translocation, and liver disease, we hypothesized that intestinal IL-17R signaling plays a critical role in mitigating hepatic inflammation. To test this, we studied intestinal epithelial-specific IL-17RA deficient mice in a model of concanavalin A hepatitis. Absence of enteric IL-17RA signaling exacerbated hepatitis and hepatocyte cell death. These mice exhibited commensal dysbiosis, increased intestinal and liver Il18, and increased liver translocation of bacterial products, specifically CpG DNA. Mechanistically, CpG DNA induced hepatic IL-18, increasing IFNγ and FasL in hepatic T-cells to drive inflammation. Thus, intestinal IL-17R regulates translocation of TLR9 ligands and constrains susceptibility to hepatitis. These data connect enteric Th17 signaling and the microbiome in hepatitis, with broader implications on the effects of impaired intestinal immunity and subsequent release of microbial products seen in other extra-intestinal pathologies.
2019-12-10 | GSE128284 | GEO
Project description:IL-17RA knockout mice presented increased tissue parasitism during T. cruzi infection that correlated with a reduced frequency of parasite-specific CD8+ T cells. Parasite-specific CD8+ T cells from KO mice showed similar proliferation rate but increased mortality and an exhausted phenotype when compared to WT counterparts. We hypothesize that during T. cruzi infection, IL-17RA signaling in CD8+ T cells is required for the regulation of a transcriptional program that prevents accelerated mortality and exhaustion and sustain the development of robust cytotoxic response required for efficient parasite control.
2020-01-31 | E-MTAB-2438 | biostudies-arrayexpress
Project description:To elucidate IL-17A-dependent immune mechanims involved in regulating host defense, we employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential of regulating protective immunity that failed to be upregulated in the absence of IL-17RA signaling. Whole small intestine tissue collected from IL-17RA-deficient and C57BL/6 (wild-type) mice was collected 2 weeks after Giardia muris infection and from uninfected controls. Expression levels of several genes that may have anti-parasitic potential (Defb1, Retnlb, Saa1, Saa2) and may be involved in parasite clearance were, on average, lower or unchanged in IL-17RA deficient compared to wild-type mice after infection. Two weeks after Giardia muris challenge, total RNA was extracted and analyzed from tissue of the small intestines of infected IL-17RA-deficient and wild-type mice, and compared to uninfected controls. Each sample contained equal amounts of total RNA from 6 female mice which were pooled and used in the experiment.
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Project description:To elucidate IL-17A-dependent immune mechanims involved in regulating host defense, we employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential of regulating protective immunity that failed to be upregulated in the absence of IL-17RA signaling. Whole small intestine tissue collected from IL-17RA-deficient and C57BL/6 (wild-type) mice was collected 2 weeks after Giardia muris infection and from uninfected controls. Expression levels of several genes that may have anti-parasitic potential (Defb1, Retnlb, Saa1, Saa2) and may be involved in parasite clearance were, on average, lower or unchanged in IL-17RA deficient compared to wild-type mice after infection.
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Project description:The upper respiratory tract (nasopharynx or NP) is the first site of influenza replication, allowing the virus to disseminate to the lower respiratory tract or promoting community transmission. The host response in the NP regulates an intricate balance between viral control and tissue pathology. The hyper-inflammatory responses promote epithelial injury, allowing for increased viral dissemination and susceptibility to secondary bacterial infections. However, the pathologic contributors to influenza upper respiratory tissue pathology are incompletely understood. In this study, we investigated the role of IL-17RA as a modulator of influenza host response and inflammation in the upper respiratory tract. We used a combined experimental approach involving IL-17RA-/- mice and an air-liquid interface (ALI) epithelial culture model to investigate the role of IL-17 response in epithelial inflammation, barrier function, and tissue pathology. Our data show that IL-17RA-/- mice exhibited significantly reduced neutrophilia, epithelial injury, and viral load. The reduced NP inflammation and epithelial injury in IL-17RA-/- mice correlated with increased resistance against co-infection by Streptococcus pneumoniae (Spn). IL-17A treatment, while potentiating the apoptosis of IAV-infected epithelial cells, caused bystander cell death and disrupted the barrier function in ALI epithelial model, supporting the in vivo findings.
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Project description:We used microarrays to compare gene expression profile of spleen CD8 T cells from IL-17RA KO and WT mice at different time-point after T. cruzi infection.
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Project description:Interleukin-23 (IL-23) and IL-17 are cytokines currently being targeted in clinical trials. Although inhibition of these cytokines is effective for treating psoriasis, IL-12/23 inhibition attenuates Crohn's disease, while IL-17A or IL-17RA inhibition exacerbates disease. This dichotomy between IL-23 and IL-17 was effectively modeled in the mdr1a- /- mouse model of colitis. IL-23 inhibition attenuated disease by decreasing colonic inflammation while enhancing Treg accumulation. Exacerbation of colitis by IL-17A or IL-17RA inhibition was associated with severe weakening of the intestinal epithelial barrier, culminating in increased colonic inflammation and accelerated mortality. These data show that IL-17A acts on intestinal epithelium to promote barrier function and provides insight into mechanisms underlying exacerbation of Crohn's disease when IL-17A or IL-17RA is inhibited.
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Project description:IL-17 is required for the initiation and progression of pancreatic cancer, particularly in the context of inflammation, as previously shown by genetic and pharmacological approaches. The cellular compartment and downstream molecular mediators of IL-17-mediated pancreatic tumorigenesis have not been fully identified. We interrogated the cellular compartment required by generating transgenic animals with Interleukin 17 receptor A (IL-17RA) genetically deleted from the pancreatic epithelial compartment vs. the hematopoietic compartment via generation of IL-17RA-deficient (IL17-RA-/-) bone marrow chimeras, in the context of embryonically activated or inducible Kras. Deletion of IL-17RA from the pancreatic epithelial compartment, but not from hematopoietic, resulted in delayed premalignant lesions initiation and progression and increased CD8+ cytotoxic T cells infiltration to the tumor microenvironment. Absence of IL-17RA in the pancreatic compartment affected transcriptional profiles of epithelial cells, modulating stemness and immunological pathways. Interestingly, B7-H4, a known inhibitor of T cell activation encoded by the gene Vtcn1, was the most upregulated checkpoint molecule via IL17 early during pancreatic tumorigenesis, and its genetic deletion delayed pancreatic premalignant lesions development and reduced immunosuppression. We reveal pancreatic epithelial IL-17RA requirement for pancreatic tumorigenesis by reprogramming the immune pancreatic landscape which is partially orchestrated by regulation of B7-H4.
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