<i>Salmonella</i> biofilms program innate immunity for persistence in <i>Caenorhabditis elegans</i>.

Abstract

The adaptive in vivo mechanisms underlying the switch in <i>Salmonella enterica</i> lifestyles from the infectious form to a dormant form remain unknown. We employed <i>Caenorhabditis elegans</i> as a heterologous host to understand the temporal dynamics of <i>Salmonella</i> pathogenesis and to identify its lifestyle form in vivo. We discovered that <i>Salmonella</i> exists as sessile aggregates, or in vivo biofilms, in the persistently infected <i>C. elegans</i> gut. In the absence of in vivo biofilms, <i>Salmonella</i> killed the host more rapidly by actively inhibiting innate immune pathways. Regulatory cross-talk between two major <i>Salmonella</i> 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.