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Gallus gallus

ABSTRACT: Early-Life Prophylactic Antibiotic Treatment Disturbed the Stability of Gut Microbiota and reduced H9N2 AIV Resistance in Chicks

PROVIDER: PRJNA880549 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24046500_1.fastq.gz	Fastqsanger.gz
	SRR24046500_2.fastq.gz	Fastqsanger.gz
	SRR24046600_1.fastq.gz	Fastqsanger.gz
	SRR24046600_2.fastq.gz	Fastqsanger.gz
	SRR24046700_1.fastq.gz	Fastqsanger.gz

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Genome-wide profiling of microRNAs revealing novel insights into mutual interactions mechanism between H9N2 avian influenza virus and avian dendritic cells

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.

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Co-infection of H9N2 influenza A virus and Escherichia coli in a BALB/c mouse model aggravates lung injury by synergistic effects

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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