Mus musculus
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ABSTRACT:
PROVIDER: PRJNA177034 | ENA |
REPOSITORIES: ENA
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Project description:Dendritic cells (DCs), professional antigen presenting cells, have demonstrated effective in controlling the initial of innate immune and enhancing immune response of vaccination, also proved that adjuvant CpG could improve the performance of immune system.Although exist many studies concerning the downstream response of DCs pulsed with CpG, rarely research gaze the interaction of DCs co-stimulated with CpG/H9N2 or CpG/inactivated H9N2 To explore the underlying molecular basis, we compared different stimulated mouse DCs with systemic approach microarrays The cultured mouse BMDCs were randomly divided into 6 groups (1: control DCs group, 2:CpG stimulated group, 3: H9N2 stimulated group, 4: CpG/H9N2 co-stimulated group, 5: inactivated H9N2 stimulated group, 6: CpG/inactivated H9N2 co-stimulated group). we used microarray to reveal striking transcriptome differences of different stimulated DCs.
2012-10-11 | E-GEOD-41454 | biostudies-arrayexpress
Project description:Background：Dendritic cells (DCs), have the most important antigen presenting ability and played an irreplaceable role in recognizing and clearing virus. Antiviral responses must rapidly defend against infection while minimizing inflammatory damage, but the mechanisms that regulate the magnitude of response within an infected cell are not well understood. MicroRNA, small non-coding RNAs, that can regulate dendritic cells to inhibit the infection and replication of avian influenza virus. Here, we global analyses how avian DCs response to H9N2 avian influenza virus (AIV) and provide a potential mechanism of how avian microRNA defending H9N2 AIV replication. Results： Here, we global analyses how avian DCs response to H9N2 avian influenza virus (AIV) and provide a potential mechanism of how avian microRNA defending H9N2 AIV replication. First, we found that both active and inactive H9N2 AIV enhance the ability of DCs to present antigens and activate T lymphocytes. Next, total microarray analyses suggested that H9N2 AIV stimulation involved in protein localization, nucleotide binding and leukocyte transendothelial migration and MAPK signal pathways. Moreover, we construct 551 transcription factor (TF)-microRNA-mRNA loops based on the above analyses. Furthermore, we found that HA fragment could not activate DCs, while truncated HA highly increased the immune function of DCs by activating ERK and STAT3 signal pathway. Last, our insight research not only gained that gga-miR1644 might target to MBNL2 to enhanced avian DCs in inhibiting virus replication, but also suggested that gga-miR6675 target to the NLS of PB1 to trigger the silencing of PB1 genes and lead to inhibition of H9N2 avian influenza viral replication. All together, our innovative research will shed new light on the roles of avian microRNA in evoking avian DCs and inhibiting virus replication, which will suggest new strategies to combat avian influenza virus.
2017-07-08 | GSE100916 | GEO
Project description:Dendritic cells (DCs), professional antigen presenting cells, have demonstrated effective in controllingthe initial of innate immune, while CpG could improve the performance of immune system. To explorethe mechanism of CpG enhancing the immune response, we compared different stimulated mouse DCswith systemic approach microarrays. Analysis revealed 1840 differentially expressed genes in H9N2stimulated group, more than 1728 altered genes in inactive H9N2 group. Investigation also proved thatCpG/inactive H9N2 co-stimulation changed 2140 genes, more than that in H9N2 group, strongly demon-strated that CpG improved the performance of inactive H9N2 vaccination. Pathways analysis founded thatDCs response rapid to shift in their maturation state, which involved Toll-like receptor (TLR) pathwaysignificantly. Microarrays results were also verified by qRT-PCR with 14 elected representative genes. Fur-ther analysis proved that co-stimulatory molecules (CD40, CD80, CD86 and MHC-II), regulatory protein(IRF-7 and TRAF-6) and pro-inflammatory cytokines (IL-1, IL-6 and IL-12) were all changed and involvedin DCs maturation. At last we demonstrated TLR signalling pathway in chicken bone marrow-deriveddendritic cells (chBM-DCs) stimulated with CpG. The distinct transcriptional profiles of DCs pulsed withvarious stimuli expanded our understanding of how DCs respond and recognize influenza.
2012-10-11 | GSE41454 | GEO
Project description:We utilize the natural cell line model (LMH and DF1) with different susceptibiltiy to H9N2 avian influenza virus to find out more and new potential key factors of influencing AIV infection and replication via a high-throughput RNA sequencing (RNA-seq).
2019-07-04 | GSE133771 | GEO
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Project description:miRNA expression patterns in immature and CpG stimulated murine BMDCs
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Project description:Pathogens that cause respiratory diseases in poultry are very complicated, and co-infections with multiple pathogens are prevalent. The H9N2 strain of avian influenza virus (AIV) and Escherichia coli (E. coli) are common poultry pathogens that limit the development of the poultry industry. This study aimed to clarify the interaction between these two pathogens and their pathogenic mechanism using a mouse model. Co-infection with H9N2 AIV and E. coli significantly increased the mortality rate of mice compared to single viral or bacterial infections. It also led to the development of more severe lung lesions compared to single viral or bacterial infections. Co-infection further causes a storm of cytokines, which aggravates the host’s disease by regulating the STAT/SOCS and ERK1/2 pathways. Moreover, co-infection mutually benefited the virus and the bacteria by increasing their multiplication rates. Importantly, nitric oxide synthase 2 (NOS2) expression was also significantly enhanced by the co-infection. It played a key role in the rapid proliferation of E. coli in the presence of the coinfecting H9N2 virus. Therefore, our study underscores the role of NOS2 as a determinant for bacteria growth and illustrates its importance as an additional mechanism that enhances influenza virus-bacteria synergy. It further provides a scientific basis for investigating the synergistic infection mechanism between viruses and bacteria.
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