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J Infect Dis. 2017 Apr 15;215(8):1245-1254. doi: 10.1093/infdis/jix141.

Enteric Helminths Promote Salmonella Coinfection by Altering the Intestinal Metabolome.

Author information

1
Michael Smith Laboratories, University of British Columbia, Vancouver.
2
Department of Biochemistry and Microbiology, University of Victoria, British Columbia.
3
Department of Microbiology and Immunology, University of British Columbia, Vancouver.
4
University of Victoria-Genome British Columbia Proteomics Centre.
5
Gerald Bronfman Department of Oncology and.
6
Proteomics Centre, Segal Cancer Centre, Lady Davis Institute, Jewish General Hospital, McGill University, Montreal, Quebec, Canada.
7
Institute of Infection, Immunity and Inflammation, University of Glasgow, United Kingdom ; and.
8
Department of Biochemistry and Molecular Biology, University of British Columbia, Vancouver, Canada.

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.

KEYWORDS:

bacterial infection; co-infection; helminths; immunomodulation; intestinal metabolites.

PMID:
28368463
PMCID:
PMC5853568
DOI:
10.1093/infdis/jix141
[Indexed for MEDLINE]
Free PMC Article

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