Cytokine and antibody response to immunization of balb c mice with e. granulosus using various routes

الملخص EN

Antibody and cytokine response were both studied in BALB / c mice immunized with Echinococcus granulose crude sheep hydrated fluid (CSHF), antigen B (AgB) and protoscoleces homogenate (PSH) via subcutaneous (sc), intraperitoneal (ip) and intramuscular (im) routes.

The present study aims at determining the most suitable antigen source and route of immunization, which stimulates the production of T helper type 1 response known to induce a protective immunity against secondary hydatidosis.

Hydrated cyst fluid (HCF, a mixture of parasite and host proteins) has led to the expansion of both IgG1 and IgG2a antibodies regardless of the immunization route.

This was accompanied with the expression of moderate IFN-γ gene in spleen cells being the highest user of im route of immunization.

Animals immunized with PSH using the ip route induced the highest IFN-γ and IL-4 gene expression, which is an indicator of a mixture of Th1 and Th2 responses.

In this group of mice, the titer of antigen specific IgG3 was significantly higher than that for the other groups.

Moreover, immunization of mice with AgB (a lipoprotein immunoregulatory component of HF) lead to high levels of IgG1 and IgG2a regardless of the route of immunization.

However, using the ip route of immunization, AgB induced higher levels of IL-4, an indication of polarization towards the Th2 response.

Immunoblotting profile showed the inability of IgG3 subclass in all groups to recognize the 16 kDa band of antigen B, whereas the reactivity to the 24 kDa band of antigen B was absent only in mice immunized ip with AgB.

In conclusion, the im route of immunization of mice with CSHF lead to high Th1 response.

While the ip immunization with PSH induced both Th1 and Th2 responses.

AgB immunization with the same route lead to dominant Th2 response.

Moreover, the IgG3 response in this model requires further investigation using cytokine gene knockout mice to elucidate the primary cytokine responsible for high IgG3 levels.