Dynamic Immune Response to Vibriosis in Pacific Oyster Crassostrea gigas Larvae during the Infection Process as Supported by Accurate Positioning of GFP-Tagged Vibrio Strains

As the immune system is not fully developed during the larval stage, hatchery culture of bivalve larvae is characterized by frequent mass mortality caused by bacterial pathogens, especially Vibrio spp. However, the knowledge is limited to the pathogenesis of vibriosis in oyster larvae, while the immune response to pathogenic microorganisms in this early life stage is still far from being fully elucidated. In this study, we combined green fluorescent protein (GFP)-tagging, histological and transcriptomic analyses to clarify the pathogenesis of experimental vibriosis and the mechanisms used by the host Pacific oyster Crassostrea gigas larvae to resist infection. The Vibrio strains first colonized the digestive system and rapidly proliferated, while only the transcription level of I kappa B kinase (IKK) and nuclear factor kappa B (NF-kappa B) associated with signaling transduction were up-regulated in oyster at 18 h post challenge (hpc). The mRNA levels for integrin beta-1, peroxinectin, and heat shock protein 70 (HSP70), which are associated with phagocytosis, cell adhesion, and cytoprotection, were not upregulated until 30 hpc when the necrosis already happened in the larval digestive system. This suggested that the immunity in the early stages of C. gigas is not strong enough to prevent vibriosis and future research may focus on the strengthening of the gastrointestinal immune ability to defend vibriosis in bivalve larvae.

Automated summary

The study found that the immunity in the early stages of Pacific oyster larvae is not strong enough to prevent vibriosis, with Vibrio strains first colonizing the digestive system and rapidly proliferating, leading to necrosis in the larval digestive system.