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人多能干细胞衍生的组织驻留巨噬细胞模型揭示了巨噬细胞对 ZIKV 和 DENV 感染的不同反应。

An hPSC-Derived Tissue-Resident Macrophage Model Reveals Differential Responses of Macrophages to ZIKV and DENV Infection.

机构信息

Department of Biological Science, Florida State University, 319 Stadium Dr., Tallahassee, FL 32306-4295, USA.

Department of Biomedical Sciences, College of Medicine, Florida State University, Tallahassee, FL 32304, USA.

出版信息

Stem Cell Reports. 2018 Aug 14;11(2):348-362. doi: 10.1016/j.stemcr.2018.06.006. Epub 2018 Jul 5.

DOI:10.1016/j.stemcr.2018.06.006
PMID:29983385
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6092684/
Abstract

Zika virus (ZIKV) and dengue virus (DENV) are two closely related flaviviruses that lead to different clinical outcomes. The mechanism for the distinct pathogenesis of ZIKV and DENV is poorly understood. Here, we investigate ZIKV and DENV infection of macrophages using a human pluripotent stem cell (hPSC)-derived macrophage model and discover key virus-specific responses. ZIKV and DENV productively infect hPSC-derived macrophages. DENV, but not ZIKV, infection of macrophages strongly activates macrophage migration inhibitory factor (MIF) secretion and decreases macrophage migration. Neutralization of MIF leads to improved migratory ability of DENV-infected macrophages. In contrast, ZIKV-infected macrophages exhibit prolonged migration and express low levels of pro-inflammatory cytokines and chemokines. Mechanistically, ZIKV disrupts the nuclear factor κB (NF-κB)-MIF positive feedback loop by inhibiting the NF-κB signaling pathway. Our results demonstrate the utility of hPSC-derived macrophages in infectious disease modeling and suggest that the distinct impact of ZIKV and DENV on macrophage immune response may underlie different pathogenesis of Zika and dengue diseases.

摘要

寨卡病毒（ZIKV）和登革热病毒（DENV）是两种密切相关的黄病毒，可导致不同的临床结果。ZIKV 和 DENV 不同发病机制的机制尚不清楚。在这里，我们使用人多能干细胞（hPSC）衍生的巨噬细胞模型研究 ZIKV 和 DENV 感染巨噬细胞，并发现关键的病毒特异性反应。ZIKV 和 DENV 可有效感染 hPSC 衍生的巨噬细胞。DENV，但不是 ZIKV，感染巨噬细胞强烈激活巨噬细胞迁移抑制因子（MIF）的分泌并减少巨噬细胞迁移。中和 MIF 可导致 DENV 感染的巨噬细胞迁移能力得到改善。相比之下，ZIKV 感染的巨噬细胞表现出延长的迁移并表达低水平的促炎细胞因子和趋化因子。从机制上讲，ZIKV 通过抑制核因子κB（NF-κB）信号通路来破坏 NF-κB-MIF 正反馈回路。我们的结果表明 hPSC 衍生的巨噬细胞在传染病建模中的实用性，并表明 ZIKV 和 DENV 对巨噬细胞免疫反应的不同影响可能是寨卡和登革热疾病不同发病机制的基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e86/6092684/89093ae7e7fe/gr7.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e86/6092684/746fb939cebf/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e86/6092684/89093ae7e7fe/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e86/6092684/52b70ba3f6a1/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e86/6092684/ed26cb0b1c9c/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e86/6092684/41b8ebf732df/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e86/6092684/6c6cc20e51e4/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e86/6092684/762413acc805/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e86/6092684/746fb939cebf/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e86/6092684/89093ae7e7fe/gr7.jpg

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