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Study of programmed cell death in bovine herpesvirus 1 infected MDBK cells and the possible role of nitric oxide in this process

机译:研究牛疱疹病毒1感染的MDBK细胞中程序性细胞死亡以及一氧化氮在此过程中的可能作用

摘要

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.ud
机译:牛疱疹病毒1(BHV-1)是许多疾病类型的病因,可能通过免疫抑制使受感染的动物易患继发性细菌感染。在某些病毒感染的细胞中,免疫抑制可能与程序性细胞死亡(PCD)的诱导直接相关。一氧化氮(NO)对真菌,细菌,原生动物,病毒病原体和肿瘤具有重要的介导作用。 BHV-1会在MDBK细胞感染后0.5-3 h(PI)之间诱导凋亡。但是,在PI 3至6 h之间,发现PCD反应降低。有趣的是,BHV-1在1小时后抑制了星形孢菌素诱导的PCD。这些结果显示与从人上皮细胞中的1型单纯疱疹感染获得的相似。施用caspase-3抑制剂后1 h PCD反应降低,而感染caspase-8和-9抑制肽后3 h NO反应升高。总之,BHV-1抑制星形孢菌素诱导的细胞凋亡反应以及NO反应。我们建议这种抑制是caspase-3依赖性的。

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