Infection Model Reveals the Critical Role of T3SS Virulence Factors in Its Pathogenicity for Sea Anemones.

is the leading cause of seafood-borne gastroenteritis. While its interaction with edible marine animals is well known, its impact on non-edible hosts remains under-explored. Using the sea anemone , we investigated pathogenicity and the role of the Type III Secretion System (T3SS). In vivo infections with a 10 CFU/mL inoculum of induced a 50% mortality rate after 7 days (LC50). Using isogenic mutant strains of with impaired key regulatory components of T3SS, impT3SS1 (CAB2), and impT3SS2 (CAB3), we demonstrated that disruption of T3SS1 significantly reduced anemone mortality. Next, we observed a time-dependent downregulation of T3SS1 effectors (VPA0450, VopQ, VopS) after 3 h and 6 h in the presence of the sea anemone, contrasting with the T3SS2-dependent VopC increased expression after 6 h. Further results support the capacity of to sense host-derived chemical cues and adjust its virulence strategies accordingly. Collectively, our findings broaden the understanding of O3:K6 as a pathogen for cnidarians and provide evidence of a major role for the T3SS1 effectors in this emerging model of host-pathogen interactions.