Chapter title |
Treatment of resistant A/J mice with methylprednisolone (MP) results in loss of resistance to murine hepatitis strain 3 (MHV-3) and induction of macrophage procoagulant activity (PCA).
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Chapter number | 12 |
Book title |
Corona- and Related Viruses
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Published in |
Advances in experimental medicine and biology, January 1995
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DOI | 10.1007/978-1-4615-1899-0_12 |
Pubmed ID | |
Book ISBNs |
978-1-4613-5775-9, 978-1-4615-1899-0
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Authors |
Fingerote, R J, Leibowitz, J L, Rao, Y S, Levy, G A, R. J. Fingerote, J. L. Leibowitz, Y. S. Rao, G. A. Levy, Fingerote, R. J., Leibowitz, J. L., Rao, Y. S., Levy, G. A. |
Abstract |
BALB/cJ mice die of fulminant hepatitis within 7 days of exposure to murine hepatitis virus strain 3 (MHV-3) whereas A/J mice are fully resistant to the lethal effects of MHV-3 infection. Previous studies have implicated macrophage activation with production of a unique macrophage prothrombinase (PCA) and lymphocyte cytokine secretion in the pathogenesis of MHV-3 susceptibility and have demonstrated that immunosuppression induces susceptibility in resistant mice. This study was undertaken to determine whether macrophages, derived from resistant A/J mice and treated in vitro with methylprednisolone sodium succinate (MP), elaborated PCA following MHV-3 exposure and whether therapy with MP altered resistance of A/J mice to MHV-3 infection in vivo. Macrophages, incubated with MP in vitro, expressed dose dependent increases in PCA following infection with MHV-3. No induction of PCA occurred in macrophages treated with MHV-3 or MP alone. Analysis of mRNA transcripts for mouse fibrinogen like protein (musfiblp), the MHV-3 specific prothrombinase, in macrophages which were incubated with MP prior to exposure to MHV-3 demonstrated significantly increased mRNA levels as compared to macrophages not incubated with MP prior to MHV-3 exposure. In vivo, A/J mice treated for 3 days with 500 mg/kg/day of MP prior to infection with MHV-3 demonstrated extensive hepatocyte necrosis and fibrin deposition in hepatic sinusoids on histological examination of liver tissue, elevated serum transaminases and 100% mortality within 10 days of infection. These results therefore provide further support for the role of increased PCA in the pathogenesis of MHV-3 related liver necrosis. |
Mendeley readers
Geographical breakdown
Country | Count | As % |
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Unknown | 16 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
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Lecturer | 2 | 13% |
Student > Bachelor | 2 | 13% |
Student > Master | 2 | 13% |
Student > Ph. D. Student | 1 | 6% |
Professor > Associate Professor | 1 | 6% |
Other | 1 | 6% |
Unknown | 7 | 44% |
Readers by discipline | Count | As % |
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Environmental Science | 1 | 6% |
Immunology and Microbiology | 1 | 6% |
Chemistry | 1 | 6% |
Other | 0 | 0% |
Unknown | 9 | 56% |