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

ABSTRACT: 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.

ORGANISM(S): Gallus gallus

PROVIDER: GSE123920 | GEO | 2020/05/28

REPOSITORIES: GEO

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Project description:Nasal cavity is the main gateway for pathogen infection although it composed of many layers of defending barriers. Pathogens strongly willing to enter and infect from nasal cavity with the dominant form aerosol or respiratory droplets. However, the underlying mechanism of virus nasal infection and transmission are still unknown. Hence, a better understanding of this mechanism may provide insight into the pathogenesis of virus. In this study, IBDV was select as a model virus to study nasal infection and transmission for it could infect chicken from head (nasal) to tail (basal) and lead to massive destruction of bursal IgM+ B-lymphocytes. Initially, we found IBDV mostly entered and infected the interior of chicken’s nasal, where full of lymphoid tissue and easily for virus to transfer into blood. After passing nasal barriers, IBDV was subsequently transmit into blood and infected PBMCs. Following blood circulates, IBDV then infected bursal and hugely destroyed B-lymphocytes. However, the mechanism of how IBDV influenced the bursal cells, especially how virus destroyed B-lymphocytes were still unclear. With the help of single cells RNA sequence, we identified five vigorous clusters, including three immune cells types (B-cells: 64.70%, dendritic cells: 3.32% and T-cells: 6.33%) and two non-immune cell types (epithelial cells: 23.86% and fibroblast cells: 1.80% cells). Further analyses found that B-cells population were serious damaged, especially IgM+ B cells. However, the IgA+ B cells population hugely increased after IBDV infection. Interesting, we first demonstrated that basal cells and other non-immune cells in Bursa of Fabricius (BF) were the main target for IBDV infection and replication. Together, our study not only comprehensive elaborated the airborne IBDV and its transmission via intranasal route into the BF, but also explained its distribution in different immune and nonimmune cells and immunoglobulins rearrangement after immunosuppressive disorder on an age dependent infected organ.