Enteric helminths promote Salmonella coinfection by altering the intestinal metabolome

Lisa A. Reynolds, Stephen A. Redpath, Sophie Yurist-Doutsch, Navkiran Gill, Eric M. Brown, Joris Van Der Heijden, Tara P. Brosschot, Jun Han, Natalie C. Marshall, Sarah E. Woodward, Yanet Valdez, Christoph H. Borchers, Georgia Perona-Wright, B. Brett Finlay

Research output: Contribution to journalArticlepeer-review

39 Citations (Scopus)

Abstract

Intestinal helminth infections occur predominantly in regions where exposure to enteric bacterial pathogens is also common. Helminth infections inhibit host immunity against microbial pathogens, which has largely been attributed to the induction of regulatory or type 2 (Th2) immune responses. Here we demonstrate an additional 3-way interaction in which helminth infection alters the metabolic environment of the host intestine to enhance bacterial pathogenicity. We show that an ongoing helminth infection increased colonization by Salmonella independently of T regulatory or Th2 cells. Instead, helminth infection altered the metabolic profile of the intestine, which directly enhanced bacterial expression of Salmonella pathogenicity island 1 (SPI-1) genes and increased intracellular invasion. These data reveal a novel mechanism by which a helminth-modified metabolome promotes susceptibility to bacterial coinfection.

Original languageEnglish
Pages (from-to)1245-1254
Number of pages10
JournalJournal of Infectious Diseases
Volume215
Issue number8
DOIs
Publication statusPublished - 2017
Externally publishedYes

Keywords

  • Bacterial infection
  • Co-infection
  • Helminths
  • Immunomodulation
  • Intestinal metabolites

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