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 IκB kinase (IKK) and nuclear factor κB (NF-κB) associated with signaling transduction were up-regulated in oyster at 18 h post challenge (hpc). The mRNA levels for integrin β-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.
Keywords: Crassostrea gigas larvae; GFP; histopathology; immune system; pathogenesis; vibriosis.