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HIV-1在人破骨细胞中复制并在体外增强其分化。

HIV-1 replicates in human osteoclasts and enhances their differentiation in vitro.

作者信息

Gohda Jin, Ma Yijing, Huang Ying, Zhang Yu, Gu Lijun, Han Yang, Li Taisheng, Gao Bin, Gao George Fu, Inoue Jun-Ichiro, Iwamoto Aikichi, Ishida Takaomi

出版信息

Retrovirology. 2015 Feb 7;12:12. doi: 10.1186/s12977-015-0139-7.

DOI:10.1186/s12977-015-0139-7
PMID:25809599
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4340110/
Abstract

BACKGROUND

HIV-1 infected patients frequently have osteolytic bone disease, which is caused by the dysregulation of the bone remodeling system that involves the interaction between osteoblasts and osteoclasts, but the relationship between osteolytic disease and HIV-1 infection remains unclear. In this study we tested whether HIV-1 infection of osteoclasts affects their differentiation.

RESULTS

We prepared human osteoclasts from CD14+ monocytes and examined them for their susceptibility to HIV-1. Furthermore, we investigated the effect of HIV-1 infection on osteoclast differentiation. CD14-derived osteoclasts were shown to express CD4, CCR5, and CXCR4 each at the similar level to that shown with macrophages. R5-tropic HIV-1 and X4-tropic HIV-1 were found to infect CD14-derived osteoclasts and replicate in them. Furthermore, HIV-1 infection induced formation of larger osteoclastst, enhanced the expression of mRNAs for three osteoclast specific marker molecules (tartrate-resistant acid phosphatase, cathepsin K, and the calcitonin receptor), and up-regulated osteoclast bone resorption activity.

CONCLUSIONS

Our results suggest that osteoclasts serve as a novel target for HIV-1 infection, which may enhance the osteoclast differentiation contributing to the development of osteolytic disease in HIV-1-infected patients.

摘要

背景

HIV-1感染患者常患有溶骨性骨病，这是由涉及成骨细胞和破骨细胞相互作用的骨重塑系统失调引起的，但溶骨性疾病与HIV-1感染之间的关系仍不清楚。在本研究中，我们测试了破骨细胞的HIV-1感染是否会影响其分化。

结果

我们从CD14+单核细胞制备了人破骨细胞，并检测了它们对HIV-1的易感性。此外，我们研究了HIV-1感染对破骨细胞分化的影响。结果显示，CD14来源的破骨细胞表达CD4、CCR5和CXCR4的水平与巨噬细胞相似。发现R5嗜性HIV-1和X4嗜性HIV-1可感染CD14来源的破骨细胞并在其中复制。此外，HIV-1感染诱导形成更大的破骨细胞，增强了三种破骨细胞特异性标记分子（抗酒石酸酸性磷酸酶、组织蛋白酶K和降钙素受体）的mRNA表达，并上调了破骨细胞的骨吸收活性。

结论

我们的结果表明，破骨细胞是HIV-1感染的新靶点，这可能会增强破骨细胞分化，导致HIV-1感染患者发生溶骨性疾病。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f14c/4340110/42c782dc052b/12977_2015_139_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f14c/4340110/513f41f3da96/12977_2015_139_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f14c/4340110/671007185fec/12977_2015_139_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f14c/4340110/a4d351d89ca5/12977_2015_139_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f14c/4340110/709786691f7f/12977_2015_139_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f14c/4340110/158f8fe47f37/12977_2015_139_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f14c/4340110/42c782dc052b/12977_2015_139_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f14c/4340110/513f41f3da96/12977_2015_139_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f14c/4340110/671007185fec/12977_2015_139_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f14c/4340110/a4d351d89ca5/12977_2015_139_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f14c/4340110/709786691f7f/12977_2015_139_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f14c/4340110/158f8fe47f37/12977_2015_139_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f14c/4340110/42c782dc052b/12977_2015_139_Fig6_HTML.jpg

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