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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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Published in: | Proceedings of the National Academy of Sciences - PNAS 2019-06, Vol.116 (25), p.12462-12467 |
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creator | Desai, Stuti K. Padmanabhan, Anup Harshe, Sharvari Zaidel-Bar, Ronen Kenney, Linda J. |
description | 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. |
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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. 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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. 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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 |
title | Salmonella biofilms program innate immunity for persistence in Caenorhabditis elegans |
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