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Mycoplasma synoviae induces serum amyloid A upregulation and promotes chicken synovial fibroblast cell proliferation

文献类型： 外文期刊

作者： Liu, Rui 1 ; Xu, Bin 1 ; Zhang, Jingfeng 1 ; Sun, Huawei 1 ; Liu, Chuanmin 1 ; Lu, Fengying 1 ; Pan, Qunxing 1 ; Zhang, X 1 ;

作者机构： 1.Jiangsu Acad Agr Sci, Inst Vet Med, Key Lab Vet Biol Engn & Technol, Minist Agr, Nanjing, Peoples R China

2.Jiangsu Acad Agr Sci, Natl Ctr Engn Res Vet Bioprod, Nanjing, Peoples R China

3.Qingdao Agr Univ, Coll Vet Med, Qingdao, Peoples R China

关键词： Mycoplasma synoviae; Chicken synovial fibroblasts; Serum amyloid A; Cell proliferation; Cell cycle

期刊名称：MICROBIAL PATHOGENESIS （ 影响因子：3.738； 五年影响因子：3.664 ）

ISSN： 0882-4010

年卷期： 2021 年 154 卷

页码：

收录情况： SCI

摘要： Mycoplasma synoviae (MS) infection causes infectious synovitis and arthritis with hyperplasia of synovial cells in the chicken joint. However, its mechanism is unknown. We used primary chicken synovial fibroblast (CSF) as the research object to study the role of MS in the proliferation of MS-infected CSF and determine the mechanisms involved. Using integrated transcriptomic and proteomic analyses of the interaction between CSF and MS, we screened a proliferation-regulated factor, serum amyloid A (SAA), that may regulate proliferation of MS-infected CSF. SAA appears to be associated with MS-induced CSF proliferation. To study the role of SAA in MS-induced CSF proliferation, a eukaryotic expression vector overexpressing SAA and a small interfering RNA (siRNA) targeting Saa were constructed to manipulate the expression of SAA. Cell proliferation and apoptosis were detected via cell counting kit-8 (CCK-8), 5-Ethynyl-2 '-deoxyuridine (EdU), or terminal deoxyribonucleotidyl transferasemediated dUTP nick-dnd labeling (TUNEL) assays, respectively. Western blot analysis was used to examine the protein expression level of SAA, cyclin E1, and cyclin-dependent kinase 2 (CDK2). In vitro, MS significantly promoted the proliferation of CSF and increased the production of SAA. Overexpression of SAA accelerated the proliferative ability of CSF, whereas knockdown of SAA depressed the proliferative ability of CSF. A TUNEL assay indicated that MS did not induce apoptosis. Silencing of SAA suppressed the expression of cyclin E1 and CDK2. These results suggest that MS may upregulate the expression of SAA, accelerate the cell cycle, and promote proliferation of CSF.

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