Species-specific mechanisms of cytotoxicity toward immune cells determine the successful outcome ofVibrioinfections

Abstract

Vibriospecies cause infectious diseases in humans and animals, but they can also live as commensals within their host tissues. HowVibriosubverts the host defenses to mount a successful infection remains poorly understood, and this knowledge is critical for predicting and managing disease. Here, we have investigated the cellular and molecular mechanisms underpinning infection and colonization of 2 virulentVibriospecies in an ecologically relevant host model, oyster, to study interactions with marineVibriospecies. AllVibriostrains were recognized by the immune system, but only nonvirulent strains were controlled. We showed that virulent strains were cytotoxic to hemocytes, oyster immune cells. By analyzing host and bacterial transcriptional responses to infection, together withVibriogene knock-outs, we discovered thatVibrio crassostreaeandVibrio tasmaniensisuse distinct mechanisms to cause hemocyte lysis. WhereasV. crassostreaecytotoxicity is dependent on a direct contact with hemocytes and requires an ancestral gene encoding a protein of unknown function,r5.7,V. tasmaniensiscytotoxicity is dependent on phagocytosis and requires intracellular secretion of T6SS effectors. We conclude that proliferation of commensal vibrios is controlled by the host immune system, preventing systemic infections in oysters, whereas the successful infection of virulent strains relies onVibriospecies-specific molecular determinants that converge to compromise host immune cell function, allowing evasion of the host immune system.