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Updated: Jul 2, 2026

An Ex Vivo Chicken Primary Bursal-cell Culture Model to Study Infectious Bursal Disease Virus Pathogenesis
Published on: October 4, 2018
Activating effects of interferons, lymphokines and viruses on cultured chicken macrophages
V Vonbulow1, H Weiler, A Klasen
1Institute of Poultry Diseases, Free University Berlin, Berlin 33, W. Germany.
Cultured chicken bone-marrow-derived and blood monocyte-derived macrophages could be activated by various treatments: (1) With crude lymphokine preparations obtained from Concanavalin A (ConA)-stimulated chicken spleen or thymus cell cultures: (2) with virus-induced interferons (IFN) from cultured chicken embryo fibroblasts or macrophages; (3) with inactivated reovirus or live infectious bursal disease virus (IBDV). Macrophage activity was expressed by cytostatic effects against lymphoblastoid target cells, and by morphological changes, such as enhanced spreading of the cells. The macrophage-activating capacity of lymphokine preparations (50% cytostasis-inducing dose) was closely associated with their antiviral activity (IFN units). According to its physico-chemical properties, ConA-induced lymphocyte interferon was considered to be IFN-gamma, but acid-and heat-resistant IFN-alpha or IFN-beta may also have been present in spleen cell or thymocyte culture supernatants. Virus-induced interferons (IFN-alpha/beta) were less effective in macrophage activation than in antiviral activity. Experimental results strongly suggested that macrophage activation by viruses was mediated by endogenous IFN.
Cultured chicken bone-marrow-derived and blood monocyte-derived macrophages could be activated by various treatments: (1) With crude lymphokine preparations obtained from Concanavalin A (ConA)-stimulated chicken spleen or thymus cell cultures: (2) with virus-induced interferons (IFN) from cultured chicken embryo fibroblasts or macrophages; (3) with inactivated reovirus or live infectious bursal disease virus (IBDV). Macrophage activity was expressed by cytostatic effects against lymphoblastoid target cells, and by morphological changes, such as enhanced spreading of the cells. The macrophage-activating capacity of lymphokine preparations (50% cytostasis-inducing dose) was closely associated with their antiviral activity (IFN units). According to its physico-chemical properties, ConA-induced lymphocyte interferon was considered to be IFN-gamma, but acid-and heat-resistant IFN-alpha or IFN-beta may also have been present in spleen cell or thymocyte culture supernatants. Virus-induced interferons (IFN-alpha/beta) were less effective in macrophage activation than in antiviral activity. Experimental results strongly suggested that macrophage activation by viruses was mediated by endogenous IFN.
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