Department of Clinical Immunology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Department of Pathogen Biology and Immunology, Shihezi University School of Medicine, Shihezi, China.
Front Immunol. 2019 Mar 12;10:96. doi: 10.3389/fimmu.2019.00096. eCollection 2019.
, a Gram-negative bacterium and the etiologic agent of plague, has evolved from , a cause of a mild enteric disease. However, the molecular and biological mechanisms of how evolved to such a remarkably virulent pathogen, , are not clear. The ability to initiate a rapid bacterial dissemination is a characteristic hallmark of infection. A distinguishing characteristic between the two species is that strains possess an O-antigen of lipopolysaccharide (LPS) while has lost the O-antigen during evolution and therefore exposes its core LPS. In this study, we showed that utilizes its core LPS to interact with SIGNR1 (CD209b), a C-type lectin receptor on antigen presenting cells (APCs), leading to bacterial dissemination to lymph nodes, spleen and liver, and the initiation of a systemic infection. We therefore propose that the loss of O-antigen represents a critical step in the evolution of into in terms of hijacking APCs, promoting bacterial dissemination and causing the plague.
鼠疫耶尔森菌是一种革兰氏阴性细菌，也是鼠疫的病原体，它由导致轻度肠道疾病的 演化而来。然而，关于 如何进化为如此致命的病原体 的分子和生物学机制尚不清楚。快速启动细菌传播的能力是 感染的一个特征标志。两种 菌株的一个显著区别在于 菌株的脂多糖（LPS）具有 O-抗原，而 在进化过程中失去了 O-抗原，因此暴露出其核心 LPS。在这项研究中，我们表明 利用其核心 LPS 与抗原呈递细胞（APCs）上的 C 型凝集素受体 SIGNR1（CD209b）相互作用，导致细菌传播到淋巴结、脾脏和肝脏，并引发全身性感染。因此，我们提出，O-抗原的缺失代表了 在劫持 APC、促进细菌传播和引起鼠疫方面， 进化为 的关键步骤。
