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The potential mechanism of concentrated mannan-oligosaccharide promoting goldfish’s (Carassius auratus Linnaeus) resistance to Ichthyophthirius multifiliis invasion

Senyue Liu,Ming Xu,Baipeng Chen,Fulong Li,Yongqiang Deng,Yufan Zhang,Gang Lin,Defang Chen,Yi Geng,Yangping Ou,Xiaoli Huang

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 concentrated mannan-oligosaccharide (cMOS) on the prevention of white spot disease in goldfish , but the specific mechanism is still unknown. In this study, transcriptome sequencing, 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 ( Carrasius auratus ) to Ich invasion. According to the transcriptome analysis, the gill tissue of goldfish receiving the cMOS diet showed greater expression of mannose-receptor (MRC) related genes, higher phagocytosis activity, up-regulated expression of phagocytosis-related genes and inflammatory-related genes compared with the control, indicating that cMOS can have an effect on phagocytosis and non-specific immunity of goldfish. After the Ich challenge, transcriptome 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 ). In conclusion, 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. The results of this study provide new insights for the mechanism of cMOS on parasitic infection, and also suggest phagocytosis-related pathways may be potential targets for prevention of Ich infection.