<i>Exaiptasia pallida</i> Infection Model Reveals the Critical Role of <i>Vibrio parahaemolyticus</i> T3SS Virulence Factors in Its Pathogenicity for Sea Anemones

<i>Exaiptasia pallida</i> Infection Model Reveals the Critical Role of <i>Vibrio parahaemolyticus</i> T3SS Virulence Factors in Its Pathogenicity for Sea Anemones

<i>Vibrio parahaemolyticus</i> 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 <i>Exaiptasia pallida</i>, we investigated <i&...

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Bibliographic Details
Main Authors: Alexandre Perrone, Estelle Bonnet, Anna Soone, Laurent Boyer, Francois Seneca
Format: Article
Language:English
Published: MDPI AG 2025-04-01
Series:Toxins
Subjects:
host–pathogen
virulence factors
secretion system
Vibrio
sea anemone
pathogenicity
Online Access:https://www.mdpi.com/2072-6651/17/4/175
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Summary:<i>Vibrio parahaemolyticus</i> 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 <i>Exaiptasia pallida</i>, we investigated <i>Vibrio parahaemolyticus</i> pathogenicity and the role of the Type III Secretion System (T3SS). In vivo infections with a 10<sup>7</sup> CFU/mL inoculum of <i>V. parahaemolyticus</i> induced a 50% mortality rate after 7 days (LC50). Using isogenic mutant strains of <i>V. parahaemolyticus</i> 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 <i>V. parahaemolyticus</i> to sense host-derived chemical cues and adjust its virulence strategies accordingly. Collectively, our findings broaden the understanding of <i>V. parahaemolyticus</i> 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.
ISSN:2072-6651

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