蛙病毒
生物
两栖动物
蝌蚪(物理学)
爪蟾
粒细胞
免疫学
非洲爪蟾
病毒
免疫系统
病毒学
微生物学
生态学
遗传学
物理
粒子物理学
基因
作者
Daphne V. Koubourli,Emily S. Wendel,Amulya Yaparla,Jonathan R. Ghaul,Leon Grayfer
标识
DOI:10.1016/j.dci.2017.02.016
摘要
Infections by Frog Virus 3 (FV3) and other ranaviruses (RVs) are contributing to the amphibian declines, while the mechanisms controlling anuran tadpole susceptibility and adult frog resistance to RVs, including the roles of polymorphonuclear granulocytes (PMNs) during anti-FV3 responses, remain largely unknown. Since amphibian kidneys represent an important FV3 target, the inability of amphibian (Xenopus laevis) tadpoles to mount effective kidney inflammatory responses to FV3 is thought to contribute to their susceptibility. Here we demonstrate that a recombinant X. laevis granulocyte colony-stimulating factor (G-CSF) generates PMNs with hallmark granulocyte morphology. Tadpole pretreatment with G-CSF prior to FV3 infection reduces animal kidney FV3 loads and extends their survival. Moreover, G-CSF-derived PMNs are resistant to FV3 infection and express high levels of TNFα in response to this virus. Notably, FV3-infected tadpoles fail to recruit G-CSFR expressing granulocytes into their kidneys, suggesting that they lack an integral inflammatory effector population at this site.
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