Because of the low host specificity, Ichthyophthirius multifiliis (Ich) can widely cause white spot disease in aquatic animals, which is extremely difficult to treat. Prior research has demonstrated a considerable impact of cMOS on the prevention of white spot disease in goldfish, but the specific mechanism is still unknown. In this study, RNA-seq, histological analysis, immunofluorescence analysis, phagocytosis activity assay and qRT-PCR assay were used to systematically reveal the potential mechanism of cMOS in supporting the resistance of goldfish to Ich invasion.
11According to RNA-seq analysis, the gill tissue of goldfish receiving cMOS diet showed greater expression of mannosereceptor (MRC) related genes, phagocytosis-related genes, inflammatory-related genes, and higher phagocytosis activity compared with the control. After Ich challenge, RNA-seq analysis revealed that cMOS fed goldfish displayed a higher level of phagocytic response, whereas non-cMOS fed goldfish displayed a greater inflammatory reaction. Besides, after Ich infection, cMOS-fed goldfish displayed greater phagocytosis activity, a stronger MRC positive signal, higher expression of genes associated with phagocytosis (ABCB2, C3, MRC), and lower expression of genes associated with inflammation (IL-1β, IL-17, IL-8, TNF-α, NFKB). Our experimental results suggest that cMOS may support phagocytosis by binding to MRC on the macrophage cell membrane and change the non- specific immunity of goldfish by stimulating cytokine expression.