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金黄色葡萄球菌和表皮葡萄球菌肠毒素 C 和 L 对小鼠肠毒性作用的分析。

Analysis of enterotoxigenic effect of Staphylococcus aureus and Staphylococcus epidermidis enterotoxins C and L on mice.

机构信息

Department of Food Hygiene and Consumer Health Protection, Wroclaw University of Environmental and Life Sciences, Wroclaw, Poland.

Hirszfeld Institute of Immunology and Experimental Therapy, Polish Academy of Sciences, Wroclaw, Poland.

出版信息

Microbiol Res. 2022 May;258:126979. doi: 10.1016/j.micres.2022.126979. Epub 2022 Feb 4.

Abstract

Pathogenic properties of orthologues to S. aureus staphylococcal enterotoxin C (SEC) and staphylococcal enterotoxin L (SEL) produced by S. epidermidis are largely unexplored. We assessed the enteropathogenic effects of S. epidermidis SEC and SEL and S. aureus SEC and SEL after oral administration to Balb/c mice. Intestinal sections from SE-treated mice were analyzed histopathologically. The T cell lineage markers (αβ and γδ TCR CD3, CD4, CD8), T-cell activation marker CD69 and proliferation-related marker CD71 were assessed in intraepithelial lymphocytes (IEL), mesenteric lymph nodes (MLN) and spleens (SPL). Serum concentrations of SEC and SEL were determined. Ortologous S. epidermidis and S. aureus SEs exerted a number of common histopathological changes in the mouse gut. Atrophy, generation of villi gap and edema of the villi were the most prominent effects of SE treatment observed in mouse gut sections. The most marked effect of ortologous S. epidermidis and S. aureus SEs on the number of goblet cells, crypt depth and villi height was noted in the mice duodenum and jejunum. We indicate early changes of TCRαβ CD4CD8a T and TCRαβ CD4CD8a T cells in response to both S. aureus and S. epidermidis SEs. Upon the treatment with SEs, markers of T cell activation and proliferation were upregulated in both αβ and γδ T cell populations derived from IEL and MLN. We demonstrated that S. epidermidis-encoded SEs applied via oral route exert pathological changes in mice gut similarly to S. aureus-encoded SEs. For the first time we indicated that SEL co-produced together with SEC by both S. aureus and S. epidermidis induces some elements of mice gut immune response and contributes to gastrointestinal tract damage. Our results indicate the potential involvement of CoNS-encoded enterotoxins in the pathogenesis of SFP.

摘要

表皮葡萄球菌产生的金黄色葡萄球菌肠毒素 C(SEC)和肠毒素 L(SEL)的同源物的致病特性在很大程度上尚未得到探索。我们评估了表皮葡萄球菌 SEC 和 SEL 以及金黄色葡萄球菌 SEC 和 SEL 经口服给药后对 Balb/c 小鼠的肠致病性作用。对 SE 处理的小鼠的肠段进行组织病理学分析。在肠上皮内淋巴细胞(IEL)、肠系膜淋巴结(MLN)和脾脏(SPL)中评估 T 细胞谱系标记物(αβ和γδ TCR CD3、CD4、CD8)、T 细胞活化标记物 CD69 和增殖相关标记物 CD71。测定血清中 SEC 和 SEL 的浓度。表皮葡萄球菌和金黄色葡萄球菌的同源 SE 对小鼠肠道产生了许多共同的组织病理学变化。在小鼠肠道切片中观察到,SE 处理最明显的作用是绒毛萎缩、绒毛间隙形成和绒毛水肿。在小鼠十二指肠和空肠中,同源表皮葡萄球菌和金黄色葡萄球菌 SE 对杯状细胞数量、隐窝深度和绒毛高度的影响最为显著。我们表明,TCRαβ CD4CD8a T 和 TCRαβ CD4CD8a T 细胞对金黄色葡萄球菌和表皮葡萄球菌 SE 的反应均存在早期变化。在用 SE 处理后,来自 IEL 和 MLN 的αβ和γδ T 细胞群体中的 T 细胞激活和增殖标记物上调。我们证明,经口服途径应用的表皮葡萄球菌编码的 SE 在小鼠肠道中引起与金黄色葡萄球菌编码的 SE 相似的病理变化。我们首次表明,金黄色葡萄球菌和表皮葡萄球菌共同产生的 SEL 与 SEC 一起诱导了小鼠肠道免疫反应的某些元素,并有助于胃肠道损伤。我们的结果表明 CoNS 编码的肠毒素可能参与 SFP 的发病机制。

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