Dengue virus selectively induces human mast cell chemokine production
Dengue virus selectively induces human mast cell chemokine production
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DOI：
10.1128/jvi.76.16.8408-8419.2002
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发表时间：
2002-08-01
影响因子：
5.4
通讯作者：
Marshall, JS
中科院分区：
文献类型：
--
作者：
King, CA;Anderson, R;Marshall, JS
严重的登革热病毒感染通常发生在已有抗登革热病毒抗体的个人身上。肥大细胞在宿主对多种病原体的防御中发挥着重要作用，但它们在病毒感染中的作用尚未阐明。研究了登革病毒感染对人肥大细胞产生趋化因子的影响。感染KU812或HMC-1人肥大细胞-嗜碱性粒细胞后，RANTES、MIP-1α和MIP-1β的分泌水平升高，而IL-8和ENA-78水平不变。在某些情况下，观察到RANTES产量增加了200倍。在未引起明显脱颗粒的条件下，脐带血来源的人肥大细胞在登革病毒特异性抗体的亚中和浓度下处理后，也显示显著增加RANTES的产生(P<；0.05)。在存在或不存在人类登革病毒特异性抗体的情况下，用紫外线灭活的登革病毒处理肥大细胞时，没有观察到趋化因子反应。无论是抗体增强型登革病毒感染高度允许的U937单核细胞系，还是腺病毒感染肥大细胞，都不会诱导RANTES、MIP-1α或MIP-1β反应，表明肥大细胞对登革病毒具有选择性反应。这些结果表明，肥大细胞在启动依赖于趋化因子的宿主对登革病毒感染的反应中发挥了作用。
Severe dengue virus infections usually occur in individuals who have preexisting anti-dengue virus antibodies. Mast cells are known to play an important role in host defense against several pathogens, but their role in viral infection has not yet been elucidated. The effects of dengue virus infection on the production of chemokines by human mast cells were examined. Elevated levels of secreted RANTES, MIP-1alpha, and MIP-1beta, but not IL-8 or ENA-78, were observed following infection of KU812 or HMC-1 human mast cell-basophil lines. In some cases a >200-fold increase in RANTES production was observed. Cord blood-derived cultured human mast cells treated with dengue virus in the presence of subneutralizing concentrations of dengue virus-specific antibody also demonstrated significantly (P < 0.05) increased RANTES production, under conditions which did not induce significant degranulation. Chemokine responses were not observed when mast cells were treated with UV-inactivated dengue virus in the presence or absence of human dengue virus-specific antibody. Neither antibody-enhanced dengue virus infection of the highly permissive U937 monocytic cell line nor adenovirus infection of mast cells induced a RANTES, MIP-1alpha, or MIP-1beta response, demonstrating a selective mast cell response to dengue virus. These results suggest a role for mast cells in the initiation of chemokine-de pendent host responses to dengue virus infection.