Hiroko Matsuyama

Protective effect of schizophyllan and scleroglucan against Streptococcus sp. infection in yellowtail (Seriola quinqueradiata)

Abstract Schizophyllan and scleroglucan, which are β-1,3-glucans derived from Schizophyllum commune and Sclerotium glucanicum, were evaluated for their ability to enhance protection against bacterial infection in yellowtail. Intraperitoneal injections of the β-1,3-glucans (2–10 mg/kg) into fish 6 and 3 days prior to intraperitoneal challenge with Streptococcus sp. resulted in a significantly increased survival rate, but the injection did not enhance resistance against Pasteurella piscicida. In β-1,3-glucan-treated fish, an elevation of serum complement and lysozyme activity was observed in addition to an increase in the phagocytic activity of pronephros cells. This suggests that the β-1,3-glucans enhanced the resistance of yellowtail against Streptococcus sp. infection through the activation of the non-specific immune system. The ineffectiveness of the β-1,3-glucans in enhancing the resistance against P. piscicida is discussed.

Opsonic effect of the third complement component (C3) of carp (Cyprinus carpio) on phagocytosis by neutrophils

The opsonic effect of carp complement on the phagocytosis by carp peritoneal neutrophils was investigated using antibody-sensitised sheep erythrocytes (EA) and bakers yeast (Y), which are the activators of the classical complement pathway (CCP) and the alternative complement pathway (ACP), respectively. Carp antibody (A) exerted little opsonic effect on the phagocytosis of sheep erythrocytes (E). The treatment of EA and Y with normal carp serum (C) greatly enhanced phagocytosis. Such opsonic effect is apparently due to the complement being activated via CCP and ACP, because the treatment of EA and Y with C3-depleted carp serum produced no effect. It was also found that the treatment of EAC and YC with the Fab fragment of anti-carp C3 (rabbit IgG) abolished the opsonising effect of carp complement deposited on the target cells. These results indicate that C3 is the major phagocytosis-promoting factor (opsonin). In addition, it was also demonstrated that pretreatment of the neutrophil surface with trypsin greatly decreased the phagocytosis of EAC, suggesting the presence of C3 receptors on the neutrophil surface.