Author:
Li Qiao,Ye Chenglin,Zhao Fei,Li Wenjin,Zhu Sizhe,Lv Yin,Park Chae Gyu,Zhang Yingmiao,Jiang Ling-Yu,Yang Kun,He Yingxia,Cai Huahua,Zhang Song,Ding Hong-Hui,Njiri Olivia Adhiambo,Tembo John Mambwe,Alkraiem Ayman Ahmad,Li An-Yi,Sun Zi-Yong,Li Wei,Yan Mei-Ying,Kan Biao,Huo Xixiang,Klena John D.,Skurnik Mikael,Anisimov Andrey P.,Gao Xiaofang,Han Yanping,Yang Rui-Fu,Xiamu Xiding,Wang Yuanzhi,Chen Hongxiang,Chai Bao,Sun Yicheng,Yuan Jingping,Chen Tie
Abstract
Yersinia pestis, the cause of plague, is a newly evolved Gram-negative bacterium. Through the acquisition of the plasminogen activator (Pla), Y. pestis gained the means to rapidly disseminate throughout its mammalian hosts. It was suggested that Y. pestis utilizes Pla to interact with the DEC-205 (CD205) receptor on antigen-presenting cells (APCs) to initiate host dissemination and infection. However, the evolutionary origin of Pla has not been fully elucidated. The PgtE enzyme of Salmonella enterica, involved in host dissemination, shows sequence similarity with the Y. pestis Pla. In this study, we demonstrated that both Escherichia coli K-12 and Y. pestis bacteria expressing the PgtE-protein were able to interact with primary alveolar macrophages and DEC-205-transfected CHO cells. The interaction between PgtE-expressing bacteria and DEC-205-expressing transfectants could be inhibited by the application of an anti-DEC-205 antibody. Moreover, PgtE-expressing Y. pestis partially re-gained the ability to promote host dissemination and infection. In conclusion, the DEC-205-PgtE interaction plays a role in promoting the dissemination and infection of Y. pestis, suggesting that Pla and the PgtE of S. enterica might share a common evolutionary origin.
Funder
National Natural Science Foundation of China
National Research Foundation of Korea
Ministry of Science and Higher Education of the Russian Federation
Natural Science Foundation of Shenzhen City
Subject
Immunology,Immunology and Allergy