| Literature DB >> 31085704 |
Chenglin Ye1, Qiao Li1, Xinyi Li2, Chae Gyu Park3, Yingxia He1, Yingmiao Zhang1, Bicong Wu1, Ying Xue1, Kun Yang4, Yin Lv1, Xiao-Ling Ying1, Hong-Hui Ding1, Huahua Cai1, Ayman Ahmad Alkraiem1,5, Olivia Njiri1, John Tembo1, Hong-Ping Huang1, An-Yi Li1, Jianping Gong1, Jichao Qin1, Bing Cheng1, Xiang Wei1, Ziyong Sun1, Shu-Sheng Zhang6, Pei Zhang6, Guo-Xing Zheng6, Wei Li7, Biao Kan7, Meiying Yan7, Xiamu Xiding8, Xixiang Huo9, Yingchun Zeng9, Hua Peng10, Yangxin Fu11, John D Klena12, Mikael Skurnik13, Ling-Yu Jiang14, Tie Chen14.
Abstract
Salmonella enterica serovar Typhimurium, a Gram-negative bacterium, can cause infectious diseases ranging from gastroenteritis to systemic dissemination and infection. However, the molecular mechanisms underlying this bacterial dissemination have yet to be elucidated. A study indicated that using the lipopolysaccharide (LPS) core as a ligand, S Typhimurium was able to bind human dendritic cell-specific intercellular adhesion molecule-3-grabbing nonintegrin (hCD209a), an HIV receptor that promotes viral dissemination by hijacking antigen-presenting cells (APCs). In this study, we showed that S Typhimurium interacted with CD209s, leading to the invasion of APCs and potentially the dissemination to regional lymph nodes, spleen, and liver in mice. Shielding of the exposed LPS core through the expression of O-antigen reduces dissemination and infection. Thus, we propose that similar to HIV, S Typhimurium may also utilize APCs via interactions with CD209s as a way to disseminate to the lymph nodes, spleen, and liver to initiate host infection.Entities:
Keywords: CD209; S. Typhimurium; dendritic cell; dissemination; lipooligosaccharide; macrophages
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Year: 2019 PMID： 31085704 PMCID： PMC6652768 DOI： 10.1128/IAI.00100-19
Source DB: PubMed Journal: Infect Immun ISSN： 0019-9567 Impact factor: 3.441