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鼠伤寒血清型沙门氏菌既可以与宿主细胞一起,也可以自主地迁移到肠系膜淋巴结。

Serovar Typhimurium Travels to Mesenteric Lymph Nodes Both with Host Cells and Autonomously.

机构信息

Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8TA, United Kingdom;

Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8TA, United Kingdom.

出版信息

J Immunol. 2019 Jan 1;202(1):260-267. doi: 10.4049/jimmunol.1701254. Epub 2018 Nov 28.

DOI:10.4049/jimmunol.1701254
PMID:30487173
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6305795/
Abstract

infection is a globally important cause of gastroenteritis and systemic disease and is a useful tool to study immune responses in the intestine. Although mechanisms leading to immune responses against have been extensively studied, questions remain about how bacteria travel from the intestinal mucosa to the mesenteric lymph nodes (MLN), a key site for Ag presentation. In this study, we used a mouse model of infection with serovar Typhimurium (STM) to identify changes in intestinal immune cells induced during early infection. We then used fluorescently labeled STM to identify interactions with immune cells from the site of infection through migration in lymph to the MLN. We show that viable STM can be carried in the lymph by any subset of migrating dendritic cells but not by macrophages. Moreover, approximately half of the STM in lymph are not associated with cells at all and travel autonomously. Within the MLN, STM associates with dendritic cells and B cells but predominantly with MLN-resident macrophages. In conclusion, we describe the routes used by STM to spread systemically in the period immediately postinfection. This deeper understanding of the infection process could open new avenues for controlling it.

摘要

感染是全球范围内引起胃肠炎和全身性疾病的重要原因,也是研究肠道免疫反应的有用工具。尽管针对 的免疫反应机制已经得到广泛研究,但仍存在一些问题,例如细菌如何从肠黏膜迁移到肠系膜淋巴结(MLN),MLN 是抗原呈递的关键部位。在这项研究中,我们使用鼠伤寒沙门氏菌(STM)感染的小鼠模型,来确定早期感染过程中诱导的肠道免疫细胞变化。然后,我们使用荧光标记的 STM 来识别从感染部位迁移到 MLN 的过程中与免疫细胞的相互作用。我们发现,活的 STM 可以被任何迁移的树突状细胞亚群携带在淋巴中,但不能被巨噬细胞携带。此外,大约一半的淋巴中的 STM 根本不与细胞结合,而是自主迁移。在 MLN 中,STM 与树突状细胞和 B 细胞结合,但主要与 MLN 驻留的巨噬细胞结合。总之,我们描述了 STM 在感染后立即向全身扩散所使用的途径。对感染过程的更深入了解可能会为控制感染开辟新的途径。

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