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Sendai virus stimulates human lung fibroblasts to release inflammatory cytokines

Karin Cebalo, Alemka Markotić, Lidija Cvetko, Ljubica Lončar, Srećko Sladoljev, Sabina Rabatić

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Abstract

Sendai virus (SeV) is a RNA virus, belongs to the family Paramyxoviridae and is pathogenic to mice. MRC-5 cells (human foetal lung fibroblasts) are suitable host cells for the propagation of numerous viruses, including Paramyxoviridae. The aim of our study was to investigate the interaction between SeV and MRC-5 cells, in relation of virus propagation and possibility to produce inflammatory cytokines/chemokines. We measured the levels of: GM-CSF, IL-6, IL-10, IL-12p70, TNF- , IFN- , IFN- , IL-8 and MCP-1. Non-infected MRC-5 cells did not produce GM-CSF, but after infection with SeV the levels increased and stayed elevated during the observation period. Non-infected MRC-5 cells produce certain amount of IL-6, IL-8 and MCP-1. While MRC-5 cells released more IL-6 and IL-8 upon the infection with SeV, the MCP-1 level was not increased. Low amounts of IFN- was detected on day 4th, while no IL-12p70, TNF- and IFN- has been detected. Acute as well as chronic human diseases has never been linked with SeV. However, the high level of replication of SeV recently observed in the upper and lower respiratory tract of nonhuman primates suggests that SeV lacks a significant host restriction in primates and could theoretically cause zoonotic disease in humans.

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What this paper is about

Sendai virus (SeV) is a RNA virus, belongs to the family Paramyxoviridae and is pathogenic to mice. MRC-5 cells (human foetal lung fibroblasts) are suitable host cells for the propagation of numerous viruses, including Paramyxoviridae. The aim of our study was to investigate the interaction between SeV and MRC-5 cells, in relation of virus propagation and possibility to produce inflammatory cytokines/chemokines. We measured the levels of: GM-CSF, IL-6, IL-10, IL-12p70, TNF- , IFN- , IFN- , IL-8 and MCP-1. Non-infected MRC-5 cells did not produce GM-CSF, but after infection with SeV the levels increased and stayed elevated during the observation period. Non-infected MRC-5 cells produce certain amount of IL-6, IL-8 and MCP-1. While MRC-5 cells released more IL-6 and IL-8 upon the infection with SeV, the MCP-1 level was not increased. Low amounts of IFN- was detected on day 4th, while no IL-12p70, TNF- and IFN- has been detected. Acute as well as chronic human diseases has never been linked with SeV. However, the high level of replication of SeV recently observed in the upper and lower respiratory tract of nonhuman primates suggests that SeV lacks a significant host restriction in primates and could theoretically cause zoonotic disease in humans.

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Available abstract

Sendai virus (SeV) is a RNA virus, belongs to the family Paramyxoviridae and is pathogenic to mice. MRC-5 cells (human foetal lung fibroblasts) are suitable host cells for the propagation of numerous viruses, including Paramyxoviridae. The aim of our study was to investigate the interaction between SeV and MRC-5 cells, in relation of virus propagation and possibility to produce inflammatory cytokines/chemokines. We measured the levels of: GM-CSF, IL-6, IL-10, IL-12p70, TNF- , IFN- , IFN- , IL-8 and MCP-1. Non-infected MRC-5 cells did not produce GM-CSF, but after infection with SeV the levels increased and stayed elevated during the observation period. Non-infected MRC-5 cells produce certain amount of IL-6, IL-8 and MCP-1. While MRC-5 cells released more IL-6 and IL-8 upon the infection with SeV, the MCP-1 level was not increased. Low amounts of IFN- was detected on day 4th, while no IL-12p70, TNF- and IFN- has been detected. Acute as well as chronic human diseases has never been linked with SeV. However, the high level of replication of SeV recently observed in the upper and lower respiratory tract of nonhuman primates suggests that SeV lacks a significant host restriction in primates and could theoretically cause zoonotic disease in humans.

Key concepts: Sendai virus, Paramyxoviridae, Virus, Chemokine, Biology, Mononegavirales, Virology, Immunology

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