MicroRNA Expression Study of chicken CD3-28-4+ intraepithelial lymphocyte natural killer cells infected with very virulent Infectious Bursal Disease Virus
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ABSTRACT:
PROVIDER: PRJNA625688 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
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| SRR11553037.fastq.gz | Fastqsanger.gz | |||
| SRR11553038.fastq.gz | Fastqsanger.gz | |||
| SRR11553039.fastq.gz | Fastqsanger.gz | |||
| SRR11553040.fastq.gz | Fastqsanger.gz | |||
| SRR11553041.fastq.gz | Fastqsanger.gz |
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Project description:Infectious bursal disease is an acute immunosuppressive viral disease which significantly affect the economic in poultry industrial. Infectious bursal disease virus (IBDV) infection was known to destroy B lymphocytes, activate macrophage and T lymphocytes, but there are limited studies on the impact of IBDV infection on chicken intraepithelial Natural killer (IEL-NK) cells. The main objective of this study is to determine the innate immune response of chicken IEL-NK cells towards very virulent IBDV (vvIBDV) infection. Specific pathogen free (SPF) chickens were infected with vvIBDV for 0, 1 and 3 dpi. The IEL-NK cells were isolated and enriched from total IEL cells using the 28.4+ antibodies. The microRNA sequencing was conducted in MiSeq system and approximately 1.6 to 3.6 million single reads generated per sample. The differential expression analysis was performed on the miRNA-Seq data. there are 35 and 16 sRNAs were differentially expressed at 1 and 3 dpi, respectively. The SNORD101, gga-miR-222a and gga-miR-221-3p were up-regulated on Day 1 and 3 whereas gga-miR-30a-50, gga-miR-142-5p, gga-miR-32-5p and gga-miR-146b-5p were down-regulated on both days. gga-miR-217-5p and gga-miR-222b-5p with the highest fold change were involved in the regulation of tumor growth and apoptosis by targeting the MAPK signaling pathway. The vvIBDV replication was suppressed by overexpression of gga-miR-21 at 3 dpi. Some of the miRNAs were up-regulated with unknown reasons but the same findings were showed in other publications such as gga-miR-3538 and gga-miR-2954 which were up-regulated after being infected by other viruses, but the roles of these miRNA are not clear.
2022-12-31 | GSE148772 | GEO
Project description:BACKGROUND:Infectious bursal disease is an acute immunosuppressive viral disease which significantly affect the economic in poultry industrial. Infectious bursal disease virus (IBDV) infection was known to destroy B lymphocytes, activate macrophage and T lymphocytes, but there are limited studies on the impact of IBDV infection on chicken intraepithelial Natural killer (IEL-NK) cells. RESULTS: The main objective of this study is to determine the innate immune response of chicken IEL-NK cells towards very virulent IBDV (vvIBDV) infection. Specific pathogen free (SPF) chickens were infected with vvIBDV for 0, 1 and 3 dpi. The IEL-NK cells were isolated and enriched from total IEL cells using the 28.4+ antibodies. The transcriptome sequencing was conducted in HiSeq2500 system and approximately 62 to 71 million paired-end reads generated per sample. The differential expression analysis was performed on the RNA-Seq data. On dpi 1, there are 838 genes up-regulated and 277 genes down-regulated. On dpi 3, there are 516 genes up-regulated whereas 750 genes down-regulated. According to pathway analysis, the differential expressed (DE) genes related to innate immune response are involved in several pathways such as cytokine-cytokine receptor, toll-like receptor and apoptosis pathway. CONCLUSION: The IEL-NK cells were de-activated after infected by vvIBDV through the down-regulation of several genes activate the NK cells such as IL18, TLR4 and TLR7/8. The IEL-NK cells were de-activated through up-regulation of expression for TGFB3 which inhibit the activation and function of NK cells by repressing the mTOR pathway. Meanwhile, the infection of vvIBDV induced apoptosis in IEL NK cells by increasing the expression level of some genes promote apoptosis such as CASP2, CASP8 and TLR3.
2020-05-28 | GSE123920 | GEO
Project description:Infectious bursal disease virus (IBDV) causes a highly contagious, immunosuppressive disease in chickens. The virus mainly infects immature B lymphocytes in the bursa of Fabricius (BF). Chicken B cell line DT40, an avian leukosis virus-induced B cell line, supports very virulent IBDV (vvIBDV) infection in vitro and thereby serves as a good model for investigating the infection and pathogenesis of this virus. However, a transcriptome-wide understanding of the interaction between vvIBDV and B cells has not yet been achieved. This study aimed to employ time-course DNA microarrays to investigate gene expression patterns in DT40 cells after infection with vvIBDV strain LX.
2016-10-01 | GSE71888 | GEO
Project description:Gene Expression Study of Innate Immune Response of Chicken Intraepithelial lymphocyte natural killer cells to very virulent Infectious Bursal Disease Virus (vvIBDV)
| PRJNA510322 | ENA
Project description:Infectious bursal disease virus strain:very virulent | isolate:BAU-MH-IBDV-BR-3 Raw sequence reads
| PRJNA998029 | ENA
Project description:The infectious bursal disease (IBD) is an acute immunosuppressive viral disease that significantly affects the economics of the poultry industry. The IBD virus (IBDV) was known to infect B lymphocytes and activate macrophage and T lymphocytes, but there are limited studies on the impact of IBDV infection on chicken intraepithelial lymphocyte natural killer (IEL-NK) cells. This study employed an mRNA sequencing approach to investigate the early regulation of gene expression patterns in chicken IEL-NK cells after infection with very virulent IBDV strain UPM0081. A total of 12,141 genes were expressed in uninfected chicken IEL-NK cells, and most of the genes with high expression were involved in the metabolic pathway, whereas most of the low expressed genes were involved in the cytokine-cytokine receptor pathway. A total of 1,266 genes were differentially expressed (DE) at 3 day-post-infection (dpi), and these DE genes were involved in inflammation, antiviral response and interferon stimulation. The innate immune response was activated as several genes involved in inflammation, antiviral response and recruitment of NK cells to the infected area were up-regulated. This is the first study to examine the whole transcriptome profile of chicken NK cells towards IBDV infection and provides better insight into the early immune response of chicken NK cells.
| S-EPMC7591896 | biostudies-literature
Project description:Due to the limitations in the range of antibodies recognising avian viruses, quantitative real-time PCR (RT-qPCR) is still the most widely used method to evaluate the expression of immunologically related genes in avian viruses. The objective of this study was to identify suitable reference genes for mRNA expression analysis in chicken intraepithelial lymphocyte natural killer (IEL-NK) cells after infection with very-virulent infectious bursal disease virus (vvIBDV). Fifteen potential reference genes were selected based on the references available. The coefficient of variation percentage (CV%) and average count of these 15 genes were determined by NanoString technology for control and infected samples. The M and V values for shortlisted reference genes (ACTB, GAPDH, HMBS, HPRT1, SDHA, TUBB1 and YWHAZ) were calculated using geNorm and NormFinder. GAPDH, YWHAZ and HMBS were the most stably expressed genes. The expression levels of three innate immune response related target genes, CASP8, IL22 and TLR3, agreed in the NanoString and RNA sequencing (RNA-Seq) results using one or two reference genes for normalisation (not HMBS). In conclusion, GAPDH and YWHAZ could be used as reference genes for the normalisation of chicken IEL-NK cell gene responses to infection with vvIBDV.
| S-EPMC7244580 | biostudies-literature
Project description:Infectious bursal disease virus (IBDV) is a highly contagious dsRNA virus (Birnaviridae) which causes immuno-suppression in chickens. Although largely controlled by vaccination, new, virulent strains of the virus mean that infectious bursal disease (IBD or ëGumboroí disease) still remains a threat to the poultry industry. The virus infects dividing IgM+ B-lymphocytes and the main site of viral replication is the bursa of Fabricius where B cells are produced. Infection is spread orally via contaminated feed and water. IBDV affects young birds, with the disease usually being diagnosed in 3-6 week old birds. Younger birds do not show clinical signs but are immuno-suppressed. Symptoms include anorexia, depression, diahorrea, ruffled feathers, immuno-suppression and bursal lesions. The disease peaks between 2-5 days post infection and is practically cleared by day 7. Mortality is variable but can be up to around 70% with very virulent strains of the disease. Even if birds survive, the resulting immuno-suppression and effect on egg production in layer birds is significant. Being able to breed commercial lines of birds for enhanced genetic resistance to IBDV is an obvious goal in the fight against the disease. Three-week-old chicks were inoculated with virus via an intra-nasal route and tissue samples were collected at 2, 3 and 4 days post-inoculation. Bursa and spleen tissues were examined from control and infected birds at 2, 3 and 4 days post-infection in birds known to be either susceptible or resistant to the virus. As well as understanding the host immune response to IBDV, we are interested in identifying genes involved in disease resistance and so we have analysed the gene expression profiles at these times, when the innate immune response is active. We assume that genes underlying resistance will be involved at this early stage of the host immune response.
2014-12-30 | E-TABM-1129 | biostudies-arrayexpress
Project description:Infectious bursal disease virus (IBDV) belongs to the family Birnaviridae and is economically important to the poultry industry worldwide. IBDV infects B cells in the bursa of Fabricius (BF), which can cause severe immunosuppression and mortality in young chickens. Earlier studies have shown that strains of IBDV lose their virulence potential after serial passage in non-B lymphoid cells, for reasons that are poorly understood. This study aimed to investigate the gene expression profiles of one cell-culture adapted attenuated IBDV strain (D78) and one very virulent IBDV strain (UK661) in chicken primary B cells cultured ex vivo from the bursa of Fabricius. The viruses were studied in B cells over 48h and their gene expression was initially evaluated with qPCR. The mRNA was isolated from the cells at 18 hours post-infection and screened with Affymetrix microarrays in triplicate. The study included mock controls which were conducted in triplicate.
2017-11-01 | E-MTAB-5947 | biostudies-arrayexpress
Project description:BackgroundInfectious bursal disease virus (IBDV) causes a highly contagious, immunosuppressive disease in chickens. The virus mainly infects immature B lymphocytes in the bursa of Fabricius (BF). Chicken B cell line DT40, an avian leukosis virus-induced B cell line, supports very virulent IBDV (vvIBDV) infection in vitro and thereby serves as a good model for investigating the infection and pathogenesis of this virus. However, a transcriptome-wide understanding of the interaction between vvIBDV and B cells has not yet been achieved. This study aimed to employ time-course DNA microarrays to investigate gene expression patterns in DT40 cells after infection with vvIBDV strain LX.ResultsDT40 cells infected with vvIBDV exhibited alterations in the expression of many important host genes involved in signal transduction pathways, including MAPK signaling, PI3K/mTOR signaling, cell death and survival, BCR signaling, and antigen presentation. The changes in cellular mRNA levels identified by microarray analysis were confirmed for 8 selected genes using real-time reverse transcription-PCR. The upregulation of inflammatory cytokines and Toll-like receptors (TLRs) in the bursa of vvIBDV-infected chickens might involve excessive activation of the innate immune and inflammatory responses and contribute to tissue damage.ConclusionsThe present study is the first to provide a comprehensive differential transcriptional profile of cultured DT40 cells in response to vvIBDV infection and further extends our understanding of the molecular mechanisms underlying vvIBDV infection and pathogenesis.
| S-EPMC5237357 | biostudies-literature