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Expression data from chicken bursal cells treated with stem cell antigen 2

ABSTRACT: The differentiation and proliferation of chicken B cells rely on the antigens on the cell surface of bursal stromal cells. Chicken stem cell antigen 2 (SCA2) is localized on the surface of bursal cortical and medullary epithelial cells. The signals through SCA2 may regulate the expressions critical for the B cell development. The altered expressions of bursal cells that were induced through SCA2-signaling were detailed via Affemetrix array experiments.

ORGANISM(S): Gallus gallus

PROVIDER: GSE18506 | GEO | 2009/10/10

SECONDARY ACCESSION(S): PRJNA118265

REPOSITORIES: GEO

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Transcription profiling of chicken bursal cells treated with stem cell antigen 2

Project description:The differentiation and proliferation of chicken B cells rely on the antigens on the cell surface of bursal stromal cells. Chicken stem cell antigen 2 (SCA2) is localized on the surface of bursal cortical and medullary epithelial cells. The signals through SCA2 may regulate the expressions critical for the B cell development. The altered expressions of bursal cells that were induced through SCA2-signaling were detailed via Affemetrix array experiments. Experiment Overall Design: Bursa of 3 week old line 0 chickens were collected and manually teased to harvest the bursal cells. The bursal cells were spread on the monolayers of SCA2Flag-DF1 cells or control Vector-DF1 cells in triplicate. After growth in the mixture of Liebovitzâs L-15 and McCoy 5A media (1:1) supplemented with 4% FBS, penicillin, and streptomycin for overnight at 37 ÂºC in 5% CO2, the bursal cells were recovered by washes (DF1 cells are adhesive) followed by gentle centrifugation at 1000Ãg for 10 min. Total RNA was isolated using the absolutely RNA microprep kit.

2009-10-20 | E-GEOD-18506 | biostudies-arrayexpress

Innate immune genes up-regulated during infectious bursal disease virus infection in chicken embryos

Project description:Next generation sequencind applied to understanding bursal disease virus infection response in chicken embryos

2022-10-21 | GSE134542 | GEO

Transcriptomics analysis of bursal B-cells from the chick embryo

Project description:The chicken bursa of Fabricius is a primary lymphoid tissue important for B-cell development. Our long-term goal is to understand the role of bursal microenvironment in an early B-cell differentiation event initiating repertoire development through immunoglobulin gene-conversion in the chick embryo. We hypothesize that early bursal B-cell differentiation is guided by signals through cytokine receptors. Our theory is based on previous evidence for expression of the receptor tyrosine kinase superfamily members and interleukin receptors in unseparated populations of bursal B-cells and bursal tissue. Knowledge of the expressed genes that are responsible for B-cell differentiation is a prerequisite for understanding the bursal microenvironment’s function. This project uses transcriptomic analysis to evaluate gene expression across early B-cell development. Approximately 90 million high quality clean reads were obtained from the cDNA libraries. The analysis revealed differentially expressed genes involved in the Jak-STAT pathway, Wnt signaling pathway, MAPK signaling pathway, metabolic pathways including tyrosine metabolism, Toll-like receptor signaling pathway, and cell-adhesion molecules. The genes predicted to encode surface receptors, signal transduction proteins and transcription factors identified in this study represent gene candidates for controlling B-cell development in response to differentiation factors in the bursal microenvironment.

2019-05-23 | GSE131652 | GEO

The severity of infectious bursal disease in White Leghorn inbred chicken lines is associated with greater bursal inflammation in vivo and more rapid induction of pro-inflammatory responses following ex vivo stimulation of primary bursal cells.

Project description:Transcriptomics analysis reveals that severity of infectious bursal disease in White Leghorn inbred chicken lines is associated with greater bursal inflammation in vivo and more rapid induction of pro-inflammatory responses following ex vivo stimulation of primary bursal cells. In order to better understand differences in the outcome of infectious bursal disease virus (IBDV) infection, we inoculated very virulent (vv) IBDV into White Leghorn chickens from inbred line W that previously had over 24% mortality, and three inbred lines (15I, C.B4 and O) that previously had 0% mortality. Within each experimental group, some individuals experienced more severe disease than others but line 15I birds experienced milder disease based on average clinical scores, percentage of birds with gross pathology, average bursal lesion scores and average peak bursal virus titre. RNA-Seq analysis revealed that more severe disease was associated with a significant up-regulation of pathways involved in inflammation, cytoskeletal regulation by Rho GTPase, nicotinic acetylcholine receptor signaling, and Wnt signaling in the bursa. Primary bursal cells cultured from line W birds and stimulated ex vivo with LPS had a more rapid up-regulation of pro-inflammatory gene expression than cells from line 15I birds, and line W birds had a significantly greater percentage of KUL01+ macrophage cells in the BF than line 15I birds. We hypothesize that a more rapid induction of pro-inflammatory cytokine responses in line W birds causes excessive inflammation and clinical disease following IBDV infection compared to line 15I, and we suggest that pro-inflammatory pathways could be targeted to engineer more disease resistant birds in the future

2021-06-02 | GSE166026 | GEO

Chicken bursal transcriptome profiling

Project description:Bursal transcriptome profiling of various chicken infected with very virulent IBDV

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Genome-wide comparison of Chicken Embryo Fibroblasts (CEF) and DF-1 in response to recombinant chicken chIFN-Î± and infection with Infectious Bursal Disease Virus (IBDV)

Project description:The spontaneously immortalised chicken DF-1 cell line is rapidly replacing its progenitor primary chicken embryo fibroblasts (CEF) in studies on avian viruses but no comprehensive study has as yet been reported comparing their immune phenotype. We conducted microarray analysis of the DF-1 and CEF, in both normal and stimulated conditions using recombinant chicken chIFN-Î± and the CEF-adapted infectious bursal disease virus vaccine strain PBG98.

2016-01-15 | E-MTAB-4028 | biostudies-arrayexpress

Evaluation of the chicken transcriptome by SAGE of B cell and the DT40 cell line

Project description:These libraries represent total RNA from bursal tissue of 20 day old CB-inbred chicks and the ALV induced bursal cell line DT40 Cre1 cells. Keywords = chicken transcriptome SAGE Bursal cell DT40 Keywords: other

2004-10-06 | GSE1817 | GEO

Genome-wide profiling of chicken DCs response to infectious bursal disease virus

Project description:Background: Avian infectious bursal disease virus (IBDV) is a major poultry disease which leads to significant losses of poultry industry. Dendritic cells (DCs), the only bridge communicated the innate and acquired immunity, have the most important antigen presenting ability and can significantly influence the pathogenicity of viruses. To understand the interaction between IBDV and DCs, microarray was used to analyze the response of DCs infected by IBDV. Results: Results showed that IBDV infection induced 479 up-regulated and 466 down-regulated mRNAs in chicken DCs. GO terms analysis suggested that transcription from RNA polymerase II promoter and RNA biosynthetic process were mainly enriched, whilst pathway analyses suggested that oxidative phosphorylation, T cell receptor and IL-17 signaling pathway might activated by IBDV infection. Moreover, we detected the microRNA (miRNA) and long non-coding RNA (lncRNA) alterations in IBDV-infected chicken DCs. Results identified 18 significant up- or down- regulated miRNAs and 441 significant up- or down-regulated lncRNAs in IBDV-stimulated DCs. Furthermore, we constructed 42 TF (transcription factors)-miRNA-mRNA interactions involving 1 TF, 3 miRNAs and 42 mRNAs in IBDV-stimulated DCs. Finally, we predicted the target genes of different expressed lncRNAs and constructed lncRNA-mRNA regulatory networks. Conclusions: Altogether, our research suggested a mechanism to explain how IBDV infection triggered an effective immune response in chicken DCs.

2016-03-24 | GSE79151 | GEO

Evaluation of the chicken transcriptome by SAGE of B cell and the DT40 cell line

2004-10-06 | E-GEOD-1817 | biostudies-arrayexpress

Gene Expression Study of Innate Immune Response of Chicken Intraepithelial lymphocyte natural killer cells to very virulent Infectious Bursal Disease Virus (vvIBDV)

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

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