Differential modulation of immune response and cytokine profiles in the bursae and spleen of chickens infected with very virulent infectious bursal disease virus

Rasoli, Mehdi; Yeap, Swee Keong; Tan, Sheau Wei; Roohani, Kiarash; Kristeen-Teo, Ye Wen; Alitheen, Noorjahan Banu Mohamed; Yasmin, Abd Rahaman; Ideris, Aini; Bejo, Mohd Hair; Kaiser, Pete; Omar, Abdul Rahman

doi:10.1186/s12917-015-0377-x

Cited by 43 publications

(26 citation statements)

References 36 publications

(57 reference statements)

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“…Moreover, both classical and vvIBDV were shown to induce apoptosis in an avian macrophage cell line, NCSU, at 72 hpi (Khatri & Sharma, 2007), and we have also recently shown that HD11 cells infected with vvIBDV strain UPM0081 undergo apoptosis after 24 hpi (Rasoli et al, 2015). In this study, we detected higher numbers of apoptotic cells in vvIBDV-infected BM-DCs compared to LPS-treated BM-DC at 12 and 24 hpi.…”

Section: Discussionsupporting

confidence: 70%

In vitrocharacterization of chicken bone marrow-derived dendritic cells following infection with very virulent infectious bursal disease virus

et al. 2015

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Infectious bursal disease is caused by infectious bursal disease virus (IBDV), an immunosuppressive virus that targets immune cells such as B cells and macrophages. However, the involvement of dendritic cells (DCs) during IBDV infection is not well understood. In this study the in vitro effects of live and inactivated very virulent IBDV (vvIBDV) UPM0081 on bone marrow-derived DCs (BM-DC) were characterized and compared with BM-DC treated with lipopolysaccharide (LPS). Morphologically, BM-DC treated with LPS and vvIBDV showed stellate shape when compared to immature BM-DC. In addition, LPS-treated and both live and inactivated vvIBDV-infected BM-DC expressed high levels of double positive CD86 and major histocompatibility complex class II antigens (>20%). vvIBDV-infected BM-DC showed significantly higher numbers of apoptotic cells compared to LPS. Replication of vvIBDV was detected in the infected BM-DC as evidenced by the increased expression of VP3 and VP4 IBDV antigens based on flow cytometry, real-time polymerase chain reaction and immunofluorescence tests. Levels of different immune-related genes such as interleukin-1β (IL-1β), CXCLi2 (IL-8), IL-18, interferon gamma (IFN-γ, IL-12α, CCR7 and Toll-like receptor-3 (TLR3) were measured after LPS and vvIBDV treatments. However, marked differences were noticed in the onset and intensity of the gene expression between these two treatment groups. LPS was far more potent than live and inactivated vvIBDV in inducing the expression of IL-1β, IL-18 and CCR7 while expression of Th1-like cytokines, IFN-γ and IL-12α were significantly increased in the live vvIBDV treatment group. Meanwhile, the expression of TLR3 was increased in live vvIBDV-infected BM-DC as compared to control. Inactivated vvIBDV-treated BM-DC failed to stimulate IFN-γ, IL-12α and TLR3 expressions. This study suggested that BM-DC may serve as another target cells during IBDV infection which require further confirmation via in vivo studies.

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Section: Discussionsupporting

confidence: 70%

In vitrocharacterization of chicken bone marrow-derived dendritic cells following infection with very virulent infectious bursal disease virus

et al. 2015

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“…Earlier expression of proinflammatory cytokines (IL-1β, IL-6, CCL4, CXCLi1) were detected in chicken spleen compared to bursa specimens [14] may also attributed to the trigger of apoptotic event in spleen isolated IgM+ cells.…”

Section: Discussionmentioning

confidence: 99%

Relationship between Virus Replication and Apoptosis Events in IgM + Cells from Chicken Spleen and Bursa of Fabricius Infected with Malaysia Strain of Very Virulent Infectious Bursal Disease Virus

Teo

Keong

Wei

et al. 2016

Acta Scientiae. Vet.

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Background: Infection of IBDV was reported to be endemic in worldwide including Malaysia and can be spread orally thru polluted fodder and water source, thus causing economic losses especially in commercial poultry industry. The infection resulted in depletion of B lymphocytes and subsequently destruction of the bursa which leaded to immunosuppression of the bird and it was postulated that the depletion of cells in the bursa was due to induction of apoptosis. In the current study, the infection of Malaysia isolated very virulent IBDV UPM0081 on IgM bearing B lymphocytes (IgM+ cells) from chicken spleen and bursa was compared. Materials, Methods & Results: A total of sixty eggs were obtained and raised until the age of 3 weeks old. The birds were divided into two groups (n = 30), which one of them served as control while IBDV strain UPM0081 was used to infect another group of birds at the concentration of 10 3 ELD50. The birds were observed and sacrificed at day 2, 4 and 5 post infections. Spleen and bursa of Fabricius were harvested and subjected to IgM+ cell enrichment using microbeads. The cell viability of enriched cells was assayed using MTT and cell cycle was analyzed using propidium iodide. Annexin V FITC and acridine orange/propidium iodide double stain assays were used to determine the event of apoptosis in the enriched IgM+ cells. Also, the IBDV viral load was also quantified by using real time PCR to evaluate the relationship between virus replication and apoptosis events in the infected chickens. Current results showed that the apoptotic events were observed to be significantly higher in IgM+ cells isolated from chicken bursa as compared to the cells isolated from spleen. The bursal B lymphocytes cell viability was observed to be decreasing following the infection of very virulent IBDV. The cells were then investigated of their apoptotic rate and data showed that increasing apoptotic cells (early and late apoptosis) were observed in AO/PI double stain as well as increment of SubG0/G1 population in the cell cycle analysis and also increment of Annexin V FITC bound cells in the apoptosis study. As for B lymphocytes from chicken spleen, the magnitude of damage caused by very virulent IBDV was not as severe as what being observed in the chicken bursa, with the cell viability drastically decreased on day 4 following IBDV infection. Discussion: IBDV caused severe destruction in bursa of Fabricius compared to spleen, in which cell death events in the former was reported to be directly caused by the virus. Apoptotic event in chicken spleen following IBDV infection was observed to be caused by oxidative stress. Thus, viral replication played a role in inducing bursal IgM+ cells death while such phenomenon was not observed in spleen isolated IgM+ cells. In summary, the cell death events of IgM+ cells in chicken spleen and bursa of Fabricius may be accounted by different factors upon infection with Malaysia strain of IBDV UPM0081. It is obvious that IgM+ cells from chicken bursa suffered from apoptotic c...

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“…CD4 and CD8 cells populations appeared to increase in the BF, decrease in the thymus (particularly in the cortex), and show an increasing trend for CD4 and decreasing CD8, which was observed in the spleen in vvIBDV infected chickens (Carballeda et al, 2014), although results from work by Rodenberg et al (1994) were contradictory. It is not clear whether these higher populations are due to cell migration from the tissues to the periphery or contractions of the resident cells (Rasoli et al, 2015). Bird age and genetic background differentially modulate the activity of T cell in IBDV infections Haase, 2005, Tippenhauer et al, 2013).…”

Section: Cd4 and Cd8 Cellsmentioning

confidence: 99%

“…IBDV increase the expression of proinflammatory cytokines IL-1, IL-6, IL-18 and inducible nitric oxide synthase iNOS in the BF (Khatri et al, 2005;Liu et al, 2010) and spleen (Palmquist et al, 2006), and significantly higher levels of nitric oxide in the splenocytes (Kim et al, 1998) and DH11 cells (Rasoli et al, 2015). Moreover, IBDV upregulate IFN-β stimulated genes, including those encoding oligoadenylate synthetase (OAS), dsRNA-dependent protein kinase (PKR), myxovirus resistance (Wong et al, 2007;Lee et al, 2015b) cyclooxygenase-2 (COX-2), chemokine (IL-8) and antigen-presenting molecules (Li et al, 2007;Lee et al, 2015b).…”

Section: Macrophagesmentioning

confidence: 99%

“…Variation in the expression of the cytokines had been noted in IBDV infection depending on the cells, virus type, age, and different tissues (He et al, 2011;Li et al, 2013a;Lee et al, 2015b;Yasmin et al, 2015). IBDV infection in chicken promotes the expression of the pro-inflammatory cytokines and chemokines, Th1 cytokines, iNOS and MHC class I in HD11 cells in vitro (Rasoli et al, 2015) and upregulate chicken IL-12 and IL-18 in HD11 cells infected with IBDV (Khatri et al, 2005;Lee et al, 2015b). IBDV also upregulates the IL-6, IL-8 and interferons (IFNs) expression in the BF (Carballeda et al, 2014) and IL-8 (Rauf et al, 2011a).…”

Section: Cytokines and Chemokinesmentioning

confidence: 99%

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Interaction of infectious bursal disease virus with the immune system of poultry

Rehman

Chen

Umar

et al. 2016

World's Poultry Science Journal

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Immune dysfunction can be either at the humoral or cellular levels and is mediated by a myriad of factors including virus-induced immunosuppression. Infectious bursal disease virus (IBDV) affects domesticated poultry and causing health problems mainly due to prolonged immunosuppression. Destruction of the immunoglobulin-producing cells is the principal cause of IBDV-induced immunosuppression, which leads to significant impairment of the primary antibody responses. Due to these effects, IBDV infection not only increases the susceptibility of poultry to other viral infections but predisposes the host to several other bacteria of variable pathologies. The IBDV-induced immunesuppression is well-known phenomenon, however, recently there have been significant advancements in understanding the molecular mechanisms of this immune-suppression. This review discuss current updates regarding the immunotoxic and immunosuppressive nature of IBDV in the poultry and highlights areas requiring future research attentions that may help to establish foundations for effective and improved vaccines against IBDV.

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Differential modulation of immune response and cytokine profiles in the bursae and spleen of chickens infected with very virulent infectious bursal disease virus

Cited by 43 publications

References 36 publications

In vitrocharacterization of chicken bone marrow-derived dendritic cells following infection with very virulent infectious bursal disease virus

In vitrocharacterization of chicken bone marrow-derived dendritic cells following infection with very virulent infectious bursal disease virus

Relationship between Virus Replication and Apoptosis Events in IgM + Cells from Chicken Spleen and Bursa of Fabricius Infected with Malaysia Strain of Very Virulent Infectious Bursal Disease Virus

Interaction of infectious bursal disease virus with the immune system of poultry

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