Salmonella enterica serovar Typhimurium travels to mesenteric lymph nodes both with host cells and autonomously

Research output: Contribution to journalArticle

Authors

  • Alberto Bravo-Blas
  • Lotta Utriainen
  • Slater L Clay
  • Verena Kästele
  • Vuk Cerovic
  • Daniel M Wall
  • Simon W F Milling

External organisations

  • Institute of Infection, Immunity and Inflammation, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow G12 8TA, United Kingdom; antonioalberto.bravo-blas@glasgow.ac.uk.
  • University of Glasgow

Abstract

Salmonella 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 Salmonella 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 Salmonella enterica 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.

Bibliographic note

Copyright © 2018 The Authors.

Details

Original languageEnglish
Pages (from-to)260-267
Number of pages8
JournalJournal of Immunology
Volume202
Issue number1
Early online date28 Nov 2018
Publication statusPublished - 1 Jan 2019