Study of programmed cell death in bovine herpesvirus 1 infected mdbk cells and the possible role of nitric oxide in this process
Autor: | Ozlem Gecer, Zafer Yazici, Huseyin Baskin, Aykut Ozkul, Yasemin Baskin, I. Hakkı Bahar |
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Přispěvatelé: | Ondokuz Mayıs Üniversitesi |
Rok vydání: | 2004 |
Předmět: |
Programmed cell death
viruses Caspase 1 Apoptosis Kidney Nitric Oxide Virus Replication Caspase 8 Cell Line Microbiology Nitric oxide chemistry.chemical_compound Animals Enzyme Inhibitors nitric oxide (NO) programmed cell death Caspase Herpesvirus 1 Bovine General Veterinary biology Caspase 3 Epithelial Cells bovine herpesvirus 1 Staurosporine biology.organism_classification Caspase Inhibitors Virology Caspase 9 Bovine herpesvirus 1 chemistry Cell culture Caspases biology.protein Cattle |
Zdroj: | Acta Veterinaria Hungarica. 52:287-297 |
ISSN: | 1588-2705 0236-6290 |
Popis: | Ozkul, Aykut/0000-0001-5008-9443; BASKIN, A. Huseyin/0000-0003-3237-267X WOS: 000223407400006 PubMed: 15379444 Bovine herpesvirus 1 (BHV-1) is the aetiological agent of many disease types and may predispose infected animals, possibly through immunosuppression, to secondary bacterial infections. Immunosuppression may directly be associated with the induction of programmed cell death (PCD) in some virus-infected cells. Nitric oxide (NO) has an important mediating role against fungal, bacterial, protozoal, viral pathogens and tumours. BHV-1 induced apoptosis between 0.5-3 h postinfection (PI) in MDBK cells; however, between 3 and 6 h PI the PCD response was found to be decreased. It was interesting to see that BHV-1 inhibited staurosporin-induced PCD after 1 h. These results showed similarities with those obtained from herpes simplex type 1 infections in human epithelial cells. PCD response decreased 1 h following caspase-3 inhibitor applications, whereas NO response increased 3 h following infection in the presence of caspase-8 and -9 inhibitory peptides. In conclusion, BHV-1 inhibited the staurosporin-induced apoptotic response and also the NO response. We propose that this inhibition is caspase-3 dependent. |
Databáze: | OpenAIRE |
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