Salmonella biofilms program innate immunity for persistence in Caenorhabditis elegans

The adaptive in vivo mechanisms underlying the switch in Salmonella enterica lifestyles from the infectious form to a dormant form remain unknown. We employed Caenorhabditis elegans as a heterologous host to understand the temporal dynamics of Salmonella pathogenesis and to identify its lifestyle fo...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2019-06, Vol.116 (25), p.12462-12467
Main Authors: Desai, Stuti K., Padmanabhan, Anup, Harshe, Sharvari, Zaidel-Bar, Ronen, Kenney, Linda J.
Format: Article
Language:English
Subjects:
Animals
Biofilms
Biological Sciences
Biomarkers - metabolism
Caenorhabditis elegans
Caenorhabditis elegans - growth & development
Caenorhabditis elegans - microbiology
Crosstalk
Immunity
Immunity, Innate - physiology
Innate immunity
Intestines - parasitology
Larva - microbiology
Nematodes
Parasitic diseases
Pathogenesis
Pathogenicity
Pathogenicity islands
Pathogens
Salmonella
Salmonella - metabolism
Salmonella - pathogenicity
Salmonella - physiology
Survival
Virulence
Worms
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Summary:The adaptive in vivo mechanisms underlying the switch in Salmonella enterica lifestyles from the infectious form to a dormant form remain unknown. We employed Caenorhabditis elegans as a heterologous host to understand the temporal dynamics of Salmonella pathogenesis and to identify its lifestyle form in vivo. We discovered that Salmonella exists as sessile aggregates, or in vivo biofilms, in the persistently infected C. elegans gut. In the absence of in vivo biofilms, Salmonella killed the host more rapidly by actively inhibiting innate immune pathways. Regulatory crosstalk between two major Salmonella pathogenicity islands, SPI-1 and SPI-2, was responsible for biofilm-induced changes in host physiology during persistent infection. Thus, biofilm formation is a survival strategy in long-term infections, as prolonging host survival is beneficial for the parasitic lifestyle.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.1822018116