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鼠源 SIGNR1(CD209b)有助于清除尿路致病性 期间尿路感染。

Murine SIGNR1 (CD209b) Contributes to the Clearance of Uropathogenic During Urinary Tract Infections.

机构信息

Department of Clinical Immunology, Tongji Hospital, Tongji Medical College, Huazhong University of Sciences and Technology, Wuhan, China.

Department of Dermatology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

出版信息

Front Cell Infect Microbiol. 2020 Jan 10;9:457. doi: 10.3389/fcimb.2019.00457. eCollection 2019.

DOI:10.3389/fcimb.2019.00457
PMID:31998663
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6965063/
Abstract

Uropathogenic (UPEC), a Gram-negative bacterial pathogen, is a major causative agent of urinary tract infections (UTIs). However, the molecular mechanisms of how UPEC causes infections have not been determined. Recent studies indicated that certain enteric Gram-negative bacteria interact with and hijack innate immune receptors DC-SIGN (CD209a) and SIGNR1 (CD209b), often expressed by antigen-presenting cells (APCs), such as macrophages, leading to dissemination and infection. It was not known whether UPEC could utilize DC-SIGN receptors to promote its infection and dissemination similarly to the enteric pathogens. The results of this study reveal that UPEC interacts with CD209-expressing macrophages and transfectants. This interaction is inhibited by anti-CD209 antibody, indicating that CD209s are receptors for UPEC. Additionally, in contrast to the results of previous studies, mice lacking SIGNR1 are more susceptible to infection of this uropathogen, leading to prolonged bacterial persistence. Overall, the results of our study indicate that the innate immune receptor CD209s participate in the clearance of UPEC during UTIs.

摘要

尿路致病性(UPEC)是一种革兰氏阴性细菌病原体,是尿路感染(UTI)的主要致病因子。然而,UPEC 引起感染的分子机制尚未确定。最近的研究表明,某些肠道革兰氏阴性细菌与先天免疫受体 DC-SIGN(CD209a)和 SIGNR1(CD209b)相互作用并劫持这些受体,这些受体通常由抗原呈递细胞(APC)表达,如巨噬细胞,导致其传播和感染。尚不清楚 UPEC 是否可以像肠道病原体一样利用 DC-SIGN 受体来促进其感染和传播。本研究的结果表明,UPEC 与表达 CD209 的巨噬细胞和转染细胞相互作用。这种相互作用被抗 CD209 抗体抑制,表明 CD209 是 UPEC 的受体。此外,与之前的研究结果相反,缺乏 SIGNR1 的小鼠更容易感染这种尿路病原体,导致细菌持续存在时间延长。总体而言,我们的研究结果表明,先天免疫受体 CD209s 参与了 UTIs 期间 UPEC 的清除。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd8f/6965063/cb45de1787a8/fcimb-09-00457-g0007.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd8f/6965063/cb45de1787a8/fcimb-09-00457-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd8f/6965063/d90e8c9f0a6f/fcimb-09-00457-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd8f/6965063/8b2c8a930acd/fcimb-09-00457-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd8f/6965063/0934d1a028f2/fcimb-09-00457-g0003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd8f/6965063/5ff13a5db958/fcimb-09-00457-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fd8f/6965063/f508fe3e4dc9/fcimb-09-00457-g0006.jpg
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