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首页> 外文期刊>Cell Health and Cytoskeleton >Keratins provide virus-dependent protection or predisposition to injury in coxsackievirus-induced pancreatitis
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Keratins provide virus-dependent protection or predisposition to injury in coxsackievirus-induced pancreatitis

机译：角蛋白为柯萨奇病毒诱发的胰腺炎的损伤提供病毒依赖的保护或易感性

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Abstract: Keratins 8 and 18 (K8/K18) are the two major intermediate filament proteins in hepatocytes and pancreatic acinar cells. Acinar cell keratins are organized as cytoplasmic and apicolateral filaments. An important role of hepatocyte K8/K18 is to maintain cellular integrity, while this cytoprotective function of K8/K18 is not evident in the pancreas since keratin-deficient mice cope well with pancreatitis models. To further study the roles of keratins in the exocrine pancreas, we used coxsackievirus B4-models, CVB4-V and CVB4-P, to induce severe acute/chronic pancreatitis and acute pancreatitis, respectively, in K8-null (which lack acinar keratins) and K18-null (which lack cytoplasmic keratins) mice. Despite similar virus titers in all mice, CVB4-V resulted in 40% mortality of the K8-null mice 14 days post-infection compared to no lethality of WT and K18-null mice. In contrast, K8-null mice were far less susceptible to CVB4-P-induced damage as determined by histology and serology analysis, and they recover faster than WT and K18-null mice. After CVB4 virus infection, keratins aggregated during acinar degranulation, and K8/K18 site-specific phosphorylation was observed during degranulation and recovery. Hence, keratins significantly affect CVB4 virulence, positively or negatively, depending on the virus subtype and keratin makeup, in a virus replication-independent manner.
机译：摘要：角蛋白8和18（K8 / K18）是肝细胞和胰腺腺泡细胞中的两个主要中间丝蛋白。腺泡细胞角蛋白组织为胞质和侧丝。肝细胞K8 / K18的重要作用是维持细胞完整性，而K8 / K18的这种细胞保护功能在胰腺中并不明显，因为缺乏角蛋白的小鼠可以很好地应对胰腺炎模型。为了进一步研究角蛋白在外分泌胰腺中的作用，我们使用了柯萨奇病毒B4-模型，CVB4-V和CVB4-P分别在K8-null（缺乏腺泡角蛋白）中诱发严重的急性/慢性胰腺炎和急性胰腺炎。和K18-null（缺少细胞质角蛋白）小鼠。尽管在所有小鼠中病毒滴度相似，但相比WT和K18无效小鼠没有致死性，CVB4-V导致感染后14天的K8无效小鼠死亡40％。相比之下，通过组织学和血清学分析确定，无K8小鼠对CVB4-P诱导的损伤的敏感性要低得多，并且其恢复速度比野生型和无K18的小鼠快。在CVB4病毒感染后，角蛋白在腺泡脱颗粒过程中聚集，并且在脱颗粒和恢复过程中观察到K8 / K18位点特异性磷酸化。因此，取决于病毒亚型和角蛋白组成，角蛋白以独立于病毒复制的方式对CVB4毒性产生正向或负面影响。

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