Specific-pathogen-free Turkey model for reoviral arthritis

Ngunjiri, John M.; Ghorbani, Amir; Jang, Hyesun; Waliullah, Sumyya; Elaish, Mohamed; Abundo, Michael C.; Kc, Mahesh; Taylor, Kara; Porter, Robert E.; Lee, Chang Won

doi:10.1016/j.vetmic.2019.06.016

Cited by 6 publications

(1 citation statement)

References 42 publications

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“…Specific pathogen free (SPF) turkeys were obtained from the Food Animal Health Research Program (OARDC, OSU) flock ( Ngunjiri et al, 2019a ) and maintained free from known turkey pathogens including reovirus, avian encephalomyelitis virus, infectious bursal disease virus, infectious bronchitis virus, Newcastle disease virus, avian influenza virus, hemorrhagic enteritis virus, Mycoplasma gallisepticum , M. synoviae , M. meleagridis , Bordetella avium and Salmonella pullorum . The turkeys were housed and acclimatized in a BSL-2 facility with forced air ventilation and adequate air exchanges to prevent ammonia build up.…”

Section: Methodsmentioning

confidence: 99%

Influenza A virus infection in turkeys induces respiratory and enteric bacterial dysbiosis correlating with cytokine gene expression

Ngunjiri

Taylor

et al. 2021

PeerJ

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Turkey respiratory and gut microbiota play important roles in promoting health and production performance. Loss of microbiota homeostasis due to pathogen infection can worsen the disease or predispose the bird to infection by other pathogens. While turkeys are highly susceptible to influenza viruses of different origins, the impact of influenza virus infection on turkey gut and respiratory microbiota has not been demonstrated. In this study, we investigated the relationships between low pathogenicity avian influenza (LPAI) virus replication, cytokine gene expression, and respiratory and gut microbiota disruption in specific-pathogen-free turkeys. Differential replication of two LPAI H5N2 viruses paralleled the levels of clinical signs and cytokine gene expression. During active virus shedding, there was significant increase of ileal and nasal bacterial contents, which inversely corresponded with bacterial species diversity. Spearman’s correlation tests between bacterial abundance and local viral titers revealed that LPAI virus-induced dysbiosis was strongest in the nasal cavity followed by trachea, and weakest in the gut. Significant correlations were also observed between cytokine gene expression levels and relative abundances of several bacteria in tracheas of infected turkeys. For example, interferon γ/λ and interleukin-6 gene expression levels were correlated positively with Staphylococcus and Pseudomonas abundances, and negatively with Lactobacillus abundance. Overall, our data suggest a potential relationship where bacterial community diversity and enrichment or depletion of several bacterial genera in the gut and respiratory tract are dependent on the level of LPAI virus replication. Further work is needed to establish whether respiratory and enteric dysbiosis in LPAI virus-infected turkeys is a result of host immunological responses or other causes such as changes in nutritional uptake.

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Section: Methodsmentioning

confidence: 99%

Influenza A virus infection in turkeys induces respiratory and enteric bacterial dysbiosis correlating with cytokine gene expression

Ngunjiri

Taylor

et al. 2021

PeerJ

Self Cite

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Infection and transmission dynamics of Turkey arthritis reovirus in different age Turkeys

Kumar

Sharafeldin

Goyal

et al. 2022

Microbial Pathogenesis

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Avian Toll-like receptor 3 isoforms and evaluation of Toll-like receptor 3–mediated immune responses using knockout quail fibroblast cells

Ngunjiri

Lee

et al. 2020

Poultry Science

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Toll-like receptor 3 ( TLR3 ) induces host innate immune response on recognition of viral double-stranded RNA ( dsRNA ). Although several studies of avian TLR3 have been reported, none of these studies used a gene knockout ( KO ) model to directly assess its role in inducing the immune response and effect on other dsRNA receptors. In this study, we determined the coding sequence of quail TLR3, identified isoforms, and generated TLR3 KO quail fibroblast ( QT-35 ) cells using a CRISPR/Cas9 system optimized for avian species. The TLR3-mediated immune response was studied by stimulating the wild-type ( WT ) and KO QT-35 cells with synthetic dsRNA or polyinosinic:polycytidylic acid [ poly(I:C )] or infecting the cells with different RNA viruses such as influenza A virus, avian reovirus, and vesicular stomatitis virus. The direct poly(I:C) treatment significantly increased IFN-β and IL-8 gene expression along with the cytoplasmic dsRNA receptor, melanoma differentiation–associated gene 5 ( MDA5 ), in WT cells, whereas no changes in all corresponding genes were observed in KO cells. We further confirmed the antiviral effects of poly(I:C)-induced TLR3-mediated immunity by demonstrating significant reduction of virus titer in poly(I:C)–treated WT cells, but not in TLR3 KO cells. On virus infection, varying levels of IFN-β, IL-8, TLR3, and MDA5 gene upregulation were observed depending on the viruses. No major differences in gene expression level were observed between WT and TLR3 KO cells, which suggests a relatively minor role of TLR3 in sensing and exerting immune response against the viruses tested in vitro. Our data show that quail TLR3 is an important endosomal dsRNA receptor responsible for regulation of type I interferon and proinflammatory cytokine, and affect the expression of MDA5, another dsRNA receptor, most likely through cytokine-mediated communication.

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Specific-pathogen-free Turkey model for reoviral arthritis

Cited by 6 publications

References 42 publications

Influenza A virus infection in turkeys induces respiratory and enteric bacterial dysbiosis correlating with cytokine gene expression

Influenza A virus infection in turkeys induces respiratory and enteric bacterial dysbiosis correlating with cytokine gene expression

Infection and transmission dynamics of Turkey arthritis reovirus in different age Turkeys

Avian Toll-like receptor 3 isoforms and evaluation of Toll-like receptor 3–mediated immune responses using knockout quail fibroblast cells

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