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Staphylococcal enterotoxin U promotes proinflammatory activity of macrophage via up‐regulation of allograft inflammatory factor 1 expression
Journal of Food Safety ( IF 2.4 ) Pub Date : 2020-01-05 , DOI: 10.1111/jfs.12765
Yanying Zhao 1 , Junni Tang 1 , Cheng Tang 1
Affiliation  

Staphylococcal enterotoxins (SEs) are a wide array of virulence factors produced by Staphylococcus aureus with potent super‐antigenic activity and they were reported to be associated with sepsis‐related infections, pneumonia, food poisoning, toxic shock syndrome, and autoimmune diseases. Macrophages play important roles in innate immune responses against bacterial infections. Thus, the present study was conducted to explore the effect of SEU on macrophage activation. Seu gene was cloned from clinical Staphylococcus aureus strain related to food poisoning; then SEU protein was purified by Ni2+ column affinity chromatography. Thereafter, macrophage proliferation was analyzed with a Cell Counting Kit‐8 and inflammatory cytokine tumor necrosis factor‐alpha (TNF‐α), interleukin 6 (IL6) secretion was assayed with the corresponding ELISA detection kit. Furthermore, western blot was used to assay inflammation‐associated protein allograft inflammatory factor 1 (AIF‐1) expression, then the expression of AIF‐1 was interfered by RNAi and the effect of SEU on macrophage proliferation and TNF‐α, IL6 secretion was assessed again. The obtained deoxynucleotide sequence of seu gene (GenBank accession No. MH737695) shared 98.5% similarity with previously identified seu from S. aureus 383F (GenBank accession No. AY205307). SEU protein‐enhanced macrophage proliferation and inflammatory cytokine TNFα, IL6 secretion. Furthermore, it upregulated AIF‐1 expression, thereafter the expression of AIF‐1 was interfered by RNAi and the interference abolished the increase of cell proliferation and inflammatory cytokine TNFα, IL6 secretion induced by SEU. Current results demonstrated that SEU promoted the proinflammatory activity of macrophage via upregulation of AIF‐1expression.

中文翻译:

金黄色葡萄球菌肠毒素U通过上调移植炎症因子1的表达促进巨噬细胞的促炎活性

金黄色葡萄球菌肠毒素(SEs)是由金黄色葡萄球菌产生的具有强大的超抗原活性的多种毒力因子,据报道与脓毒症相关感染,肺炎,食物中毒,中毒性休克综合征和自身免疫性疾病有关。巨噬细胞在针对细菌感染的先天免疫反应中起重要作用。因此,进行本研究以探讨SEU对巨噬细胞活化的作用。从与食物中毒有关的临床金黄色葡萄球菌菌株中克隆了Seu基因。然后用Ni 2+纯化SEU蛋白柱亲和色谱。之后,使用细胞计数试剂盒-8和炎症细胞因子肿瘤坏死因子α(TNF-α)分析巨噬细胞增殖,并使用相应的ELISA检测试剂盒分析白细胞介素6(IL6)分泌。此外,蛋白质印迹法用于检测炎症相关蛋白同种异体移植炎症因子1(AIF-1)的表达,然后RNAi干扰AIF-1的表达,SEU对巨噬细胞增殖和TNF-α,IL6分泌的影响为再次评估。将得到的脱氧核苷酸序列SEU基因(GenBank登录号MH737695)共享98.5%的相似性与先前识别的SEU小号金黄色383F(GenBank登录号AY205307)。SEU蛋白增强巨噬细胞增殖和炎性细胞因子TNFα,IL6分泌。此外,它上调了AIF-1的表达,此后AIF-1的表达受到RNAi的干扰,这种干扰消除了SEU诱导的细胞增殖和炎性细胞因子TNFα,IL6分泌的增加。当前结果表明,SEU通过上调AIF-1表达来促进巨噬细胞的促炎活性。
更新日期:2020-01-05
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