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首页> 外文期刊>Journal of Medical Microbiology: An Official Journal of the Pathological Society of Great Britain and Ireland >Loss of the virulence plasmid by Shigella sonnei promotes its interactions with CD207 and CD209 receptors
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Loss of the virulence plasmid by Shigella sonnei promotes its interactions with CD207 and CD209 receptors

机译：<斜视> shigella sonnei 损失毒力质粒促进其与CD207和CD209受体的相互作用

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Introduction Shigella sonnei, the cause of bacillary dysentery, belongs to Gram-negative enteropathogenic bacteria. S. sonnei contains a 210?kb virulence plasmid that encodes an O-antigen gene cluster of LPSs. However, this virulence plasmid is frequently lost during replication. It is well-documented that after losing the O-antigen and becoming rough strains, the Gram-negative bacteria may express an LPS core on its surface. Previous studies have suggested that by using the LPS core, Gram-negative bacteria can interact with several C-type lectin receptors that are expressed on antigen-presenting cells (APCs). Hypothesis/Gap Statement S. sonnei by losing the virulence plasmid may hijack APCs via the interactions of LPS-CD209/CD207. Aim This study aimed to investigate if the S. sonnei rough strain, by losing the virulence plasmid, interacted with APCs that express C-type lectins of human CD207, human CD209a and mouse CD209b. Methodology SDS-PAGE silver staining was used to examine the O-antigen expression of S. sonnei WT and its rough strain. Invasion assays and inhibition assays were used to examine the ability of S. sonnei WT and its rough strain to invade APCs and investigate whether CD209 and CD207 are receptors for phagocytosis of rough S. sonnei . Animal assays were used to observe the dissemination of S. sonnei . Results S. sonnei did not express O-antigens after losing the virulence plasmid. The S. sonnei rough strain invades with APCs, including human dendritic cells (DCs) and mouse macrophages. CD209 and CD207 are receptors for phagocytosis of rough S. sonnei . Expression of the O-antigen reduces the ability of the S. sonnei rough strain to be disseminated to mesenteric lymph nodes and spleens. Conclusion This work demonstrated that S. sonnei rough strains – by losing the virulence plasmid – invaded APCs through interactions with CD209 and CD207 receptors.
机译：简介Shigella Sonnei，Bacillary Dysentery的原因属于革兰癌致癌细菌。 S. Sonnei含有210？KB毒力质粒，编码LPS的O-抗原基因组。然而，这种毒力质粒经常在复制过程中丢失。它有良好的记录，在失去O-抗原并变得粗糙的菌株后，革兰氏阴性细菌可以在其表面上表达LPS核心。以前的研究表明，通过使用LPS核心，革兰氏阴性细菌可以与在抗原呈递细胞（APC）上表达的几种C型凝集素受体相互作用。通过失去毒力质粒来通过LPS-CD209 / CD207的相互作用来迁移毒力质粒来解析SONNEIS。目的本研究旨在调查S. Sonnei粗菌，通过丧失毒力质粒，与表达人CD207，人CD209a和小鼠CD209b的C型凝集素的APC相互作用。方法学SDS-PAGE银染色用于检查S. sonnei wt及其粗菌株的O-抗原表达。侵袭测定和抑制测定用于检测S. Sonnei WT及其粗菌菌侵入APC的能力，并研究CD209和CD207是否是粗糙S. Sonnei的吞噬作用的受体。动物测定用于观察S. Sonnei的传播。结果S.Sonnei在失去毒力质粒后没有表达O-抗原。 S. Sonnei粗菌侵入APC，包括人树突细胞（DCS）和小鼠巨噬细胞。 CD209和CD207是粗糙S. Sonnei的吞噬作用的受体。 O-抗原的表达降低了S. Sonnei粗菌菌散发到肠系膜淋巴结和脾脏的能力。结论这项工作证明了S. Sonnei粗菌株 - 通过与CD209和CD207受体的相互作用失去毒力质粒侵袭的APC。

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