Role of vascular and lymphatic endothelial cells in hantavirus pulmonary syndrome suggests targeted therapeutic approaches.
Role of vascular and lymphatic endothelial cells in hantavirus pulmonary syndrome suggests targeted therapeutic approaches.
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DOI：
10.1089/lrb.2013.0006
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发表时间：
2013-09
影响因子：
1.4
通讯作者：
E. Mackow;E. Gorbunova;Nadine A. Dalrymple;I. Gavrilovskaya
中科院分区：
文献类型：
--
作者：
E. Mackow;E. Gorbunova;Nadine A. Dalrymple;I. Gavrilovskaya
背景汉坦病毒在美洲引起高度致死性的急性肺水肿，称为汉坦病毒肺综合征（HPS）。汉坦病毒非溶解性感染微血管和淋巴管内皮细胞，并引起屏障功能的显着变化，而不破坏内皮。汉坦病毒引起受感染的内皮细胞功能的变化，这些内皮细胞通常调节液体屏障功能。动脉、静脉和淋巴管的内皮对于调节肺液体积聚的巨大肺毛细血管床的功能是独特的和中心的。结果我们已经发现，HPS引起的汉坦病毒通过改变受体和信号通路反应，改变微血管和淋巴管内皮细胞的血管屏障功能，从而允许液体组织流入和清除组织水肿。内皮细胞的感染为汉坦病毒引起急性肺水肿提供了多种机制，也为降低HPS疾病严重程度提供了潜在的治疗靶点。结论：在这里，我们讨论了引起HPS的汉坦病毒与内皮的相互作用，独特的淋巴管内皮反应在HPS中的作用，以及作为降低HPS疾病严重程度的一种手段的内皮治疗靶向。
BACKGROUND Hantaviruses in the Americas cause a highly lethal acute pulmonary edema termed hantavirus pulmonary syndrome (HPS). Hantaviruses nonlytically infect microvascular and lymphatic endothelial cells and cause dramatic changes in barrier functions without disrupting the endothelium. Hantaviruses cause changes in the function of infected endothelial cells that normally regulate fluid barrier functions. The endothelium of arteries, veins, and lymphatic vessels are unique and central to the function of vast pulmonary capillary beds that regulate pulmonary fluid accumulation. RESULTS We have found that HPS-causing hantaviruses alter vascular barrier functions of microvascular and lymphatic endothelial cells by altering receptor and signaling pathway responses that serve to permit fluid tissue influx and clear tissue edema. Infection of the endothelium provides several mechanisms for hantaviruses to cause acute pulmonary edema, as well as potential therapeutic targets for reducing the severity of HPS disease. CONCLUSIONS Here we discuss interactions of HPS-causing hantaviruses with the endothelium, roles for unique lymphatic endothelial responses in HPS, and therapeutic targeting of the endothelium as a means of reducing the severity of HPS disease.