Newcastle disease virus infection in chicken embryonic fibroblasts but not duck embryonic fibroblasts is associated with elevated host innate immune response

Abstract

BackgroundChickens and ducks are major hosts of Newcastle disease virus (NDV) with distinct responses to infection. However, whereas ducks are generally asymptomatic or exhibit only mild symptoms following NDV infection and are thus regarded as potential long-term reservoirs of the virus, chickens exhibit severe clinical lesions, transient infections and even death due to NDV infection. These differences may in part result from the host innate immune response to NDV infection.MethodsTo better understand the host innate immune response to NDV infection in avian species, by using the quantitative real-time polymerase chain reaction method we examined the messenger RNA expression levels of immune-related genes in chicken embryonic fibroblasts (CEFs) and duck embryonic fibroblasts (DEFs) when infected with NDV of different pathogenicities.ResultsGene expression profiles showed that the expression of IL-1beta, TNF-α-like factor (LITAF) and interferon (IFN)-beta was upregulated in both CEFs and DEFs infected with SS-10 and NH-10 viruses or treated with polyinosinic:polycytidylic acid [poly(I:C)], as well as that expression levels were greater in CEFs than in DEFs. The expression of TLR3, TLR7, IL-6, IFN-alpha, IFN-gamma, MHC-I and MHC-II, except for IL-8, were also greater in CEFs than in DEFs in response to infection to both viruses or treatment with poly(I:C). However, unlike moderate virulent NH-10, highly virulent SS-10 induced greater pattern recognition receptors and cytokines, except for IFNs, in CEFs and DEFs.ConclusionResults show distinct expression patterns of cytokines, Toll-like receptors and IFNs associated with inflammatory immune responses to NDV between species and by virulence.

IFN-γ establishes interferon-stimulated gene-mediated antiviral state against Newcastle disease virus in chicken fibroblasts

“…The expressions of crucial genes, including TLR3, TLR7, IL1B, IRF7, IL8, STAT1, and MHC class I and II molecules, are characteristic of NDV infection in chicken cells. However, in previously performed studies, a significant expression of type I IFNs (INF-α and IFN-β) was observed against NDV infection [53,54]. Surprisingly, in our experimental settings, we were unable to observe this response.…”

“…Major genes including IL1β, IL6, IL8, CCL4, CCL5, STAT1, TLR3, IRF7, IFITM-1, IFITM-3, IFITM-5, STAT1, NF-kB, MX1, RSAD2 (viperin), MDA5, and ZAP were identified in this study ( Supplementary Table S1). Interestingly, among all those crucial genes related to innate immunity identified in the present study, we found that TLR3, TLR7, IL1B, IRF7, IL8, STAT1, and MHC class I and II molecules are exactly the same as those observed in previously studies where similar gene expression was shown in CEFs treated with NDV (genotype VII and IX) [53,54]. In short, our results demonstrated a low level (nonsignificant) expression of IFN-α and IFN-β.…”

“…It has recently been shown that chIFN-γ induces ISGs and sustains a potent antiviral environment in host cells [58]. Interestingly, all three types of chicken IFNs (IFN-α, IFN-β, and IFN-γ) are upregulated in response to NDV infection [53]. However, upon infection with velogenic NDV, IFN-γ is significantly upgraded in the bursa of Fabricius, while expression of IFN-γ does not markedly reduce the proliferation and replication of NDV in vitro [26,59].…”

“…Surprisingly, in our experimental settings, we were unable to observe this response. This may be due to multiple reasons, including the use of different viral genotypes, the origin and source of virus, and the type of cells used to determine the NDV-mediated pathogenesis in different bird species [53]. Collectively, based on our experimental findings, we can postulate that the temporal induction of IFNs in response to NDV infection in CEFs is dependent on certain factors, including viral genotype, viral source, cell type, mode of infection, and time points of NDV infection in cells.…”

In vitro estimation of metal-induced disturbance in chicken gut-oviduct chemokine circuit

“…Moreover, induced pluripotency in chicken eF can generate germ cells and facilitate their optimal survival and migration to embryonic gonads via the chemokine receptor-linked pathway 19,20 . in addition to impacts on egg development, eF can play key roles in the innate immunological recognition and tissue repair following infection and inflammatory insults to the reproductive organs [21][22][23] . in the present study, eFs were used to compare the relative toxicities of inorganic heavy metals, which are known to contaminate mammalian and avian diets as well as drinking water.…”