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The chemokines CCL2 and CXCL10 produced by bovine endometrial epithelial cells induce migration of bovine B lymphocytes, contributing to transuterine transmission of BLV infection.
Veterinary Microbiology ( IF 2.4 ) Pub Date : 2020-01-28 , DOI: 10.1016/j.vetmic.2020.108598
Kiyohiko Andoh 1 , Asami Nishimori 1 , Ryosuke Sakumoto 2 , Ken-Go Hayashi 2 , Shinichi Hatama 1
Affiliation  

Bovine leukemia virus (BLV) causes a lymphoproliferative disease in cattle and is transmitted horizontally and vertically via infected lymphocytes. Although transplacental infection is considered the predominant route of vertical transmission of BLV, the molecular mechanisms of this process remain to be elucidated. Notably, how BLV passes through the blood-placental barrier remains unclear, given that BLV is transmitted primarily by cell-to-cell contact. One hypothesis is that B cell migration to the placenta may be induced by certain endometrium-expressed chemokines. To test this hypothesis, we performed an in vitro cell migration assay using bovine B cell lines and endometrial epithelial cells. Cell migration assays showed that two bovine B cell lines, BL2M3 and BL3.1 cells, were attracted to the supernatant of bovine endometrial epithelial cells (BEnEpCs). Quantitative real-time RT-PCR showed that expression levels of mRNAs encoding the chemokines CCL2 and CXCL10 were higher in BEnEpCs than in MDBK cells. Additionally, an inhibition assay using immune serum against CCL2 and CXCL10 showed suppression of migration of bovine B cell lines. A syncytium assay showed that cells expressing BLV envelope (Env) protein fused with BEnEpCs. Here we found that bovine B cells are attracted by chemokines produced in the endometrium and that cells expressing BLV Env protein fused with endometrium epithelial cells. These results explain part of the molecular mechanism of transplacental transmission during BLV infection, although further analysis will be required. Advances in these areas are expected to contribute to controlling the spread of BLV.

中文翻译:

牛子宫内膜上皮细胞产生的趋化因子CCL2和CXCL10诱导牛B淋巴细胞迁移,从而促进BLV感染的经子宫传播。

牛白血病病毒(BLV)引起牛的淋巴增生性疾病,并通过感染的淋巴细胞水平和垂直传播。尽管经胎盘感染被认为是BLV垂直传播的主要途径,但该过程的分子机制仍有待阐明。值得注意的是,鉴于BLV主要通过细胞间接触传播,因此BLV如何通过血胎盘屏障尚不清楚。一种假设是B细胞迁移到胎盘可能是由某些子宫内膜表达的趋化因子诱导的。为了验证该假设,我们使用牛B细胞系和子宫内膜上皮细胞进行了体外细胞迁移试验。细胞迁移分析表明,有两种牛B细胞系BL2M3和BL3.1细胞,牛子宫内膜上皮细胞(BEnEpCs)的上清液被吸引。实时定量RT-PCR显示,BEnEpC中编码趋化因子CCL2和CXCL10的mRNA的表达水平高于MDBK细胞。此外,使用针对CCL2和CXCL10的免疫血清进行的抑制分析显示,牛B细胞系迁移受到抑制。合胞体检测显示,表达BLV包膜(Env)蛋白的细胞与BEnEpCs融合。在这里,我们发现牛B细胞被子宫内膜中产生的趋化因子吸引,并且表达BLV Env蛋白的细胞与子宫内膜上皮细胞融合。这些结果解释了BLV感染期间经胎盘传播的分子机制的一部分,尽管将需要进一步的分析。
更新日期:2020-01-28
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