Atypical salmonella enterica serovars in murine and human macrophage infection models

Daniel Hurley*, Maria Hoffmann, Tim Muruvanda, Marc W. Allard, Eric W. Brown, Marta Martins, Séamus Fanning

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)

Abstract

Nontyphoidal Salmonella species are globally disseminated pathogens and are the predominant cause of gastroenteritis. The pathogenesis of salmonellosis has been extensively studied using in vivo murine models and cell lines, typically challenged with Salmonella enterica serovar Typhimurium. Although S. enterica serovars Enteritidis and Typhimurium are responsible for most of the human infections reported to the Centers for Disease Control and Prevention (CDC), several other serovars also contribute to clinical cases of salmonellosis. Despite their epidemiological importance, little is known about their infection phenotypes. Here, we report the virulence characteristics and genomes of 10 atypical S. enterica serovars linked to multistate foodborne outbreaks in the United States. We show that the murine RAW 264.7 macrophage model of infection is unsuitable for inferring human-relevant differences in nontyphoidal Salmonella infections, whereas differentiated human THP-1 macrophages allowed these isolates to be further characterized in a more humanrelevant context.

Original languageEnglish
Article numbere00353-19
JournalInfection and Immunity
Volume88
Issue number4
DOIs
Publication statusPublished - 23 Mar 2020
Externally publishedYes

Bibliographical note

Publisher Copyright:
© 2020 American Society for Microbiology. All rights reserved.

Keywords

  • Cytokines
  • Infection
  • Macrophages
  • Pathogenicity
  • Salmonella
  • Salmonella enterica
  • Virulence
  • Whole-genome sequencing

ASJC Scopus subject areas

  • Parasitology
  • Microbiology
  • Immunology
  • Infectious Diseases

Fingerprint

Dive into the research topics of 'Atypical salmonella enterica serovars in murine and human macrophage infection models'. Together they form a unique fingerprint.

Cite this