Department of Clinical Immunology, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan, Hubei, PR China.
Henan Provincial Center for Disease Control and Prevention, Zhengzhou, Henan, PR China.
J Med Microbiol. 2021 Mar;70(3). doi: 10.1099/jmm.0.001297. Epub 2021 Feb 16.
the cause of bacillary dysentery, belongs to Gram-negative enteropathogenic bacteria. 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). by losing the virulence plasmid may hijack APCs via the interactions of LPS-CD209/CD207. This study aimed to investigate if the rough strain, by losing the virulence plasmid, interacted with APCs that express C-type lectins of human CD207, human CD209a and mouse CD209b. SDS-PAGE silver staining was used to examine the O-antigen expression of WT and its rough strain. Invasion assays and inhibition assays were used to examine the ability of WT and its rough strain to invade APCs and investigate whether CD209 and CD207 are receptors for phagocytosis of rough . Animal assays were used to observe the dissemination of . did not express O-antigens after losing the virulence plasmid. The rough strain invades with APCs, including human dendritic cells (DCs) and mouse macrophages. CD209 and CD207 are receptors for phagocytosis of rough . Expression of the O-antigen reduces the ability of the rough strain to be disseminated to mesenteric lymph nodes and spleens. This work demonstrated that rough strains - by losing the virulence plasmid - invaded APCs through interactions with CD209 and CD207 receptors.
细菌性痢疾的病因属于革兰氏阴性肠道致病菌。它含有一个 210kb 的毒力质粒，该质粒编码 LPS 的 O-抗原基因簇。然而，这种毒力质粒在复制过程中经常丢失。有充分的证据表明，在失去 O-抗原并成为粗糙菌株后，革兰氏阴性菌可能在其表面表达 LPS 核心。先前的研究表明，通过使用 LPS 核心，革兰氏阴性菌可以与表达在抗原呈递细胞 (APC) 上的几种 C 型凝集素受体相互作用。通过失去毒力质粒，可能通过 LPS-CD209/CD207 的相互作用劫持 APC。本研究旨在探讨失去毒力质粒的 粗糙菌株是否与表达人 CD207、人 CD209a 和小鼠 CD209b 的 APC 相互作用。SDS-PAGE 银染用于检测 WT 及其粗糙菌株的 O-抗原表达。侵袭实验和抑制实验用于检测 WT 及其粗糙菌株入侵 APC 的能力，并研究 CD209 和 CD207 是否是吞噬粗糙的受体。动物实验用于观察 的传播。失去毒力质粒后， 不再表达 O-抗原。粗糙菌株与 APC 一起入侵，包括人树突状细胞 (DC) 和小鼠巨噬细胞。CD209 和 CD207 是吞噬粗糙 的受体。O-抗原的表达降低了 粗糙菌株传播到肠系膜淋巴结和脾脏的能力。这项工作表明，通过失去毒力质粒， 粗糙菌株通过与 CD209 和 CD207 受体相互作用而入侵 APC。
