Data/hora: 11/06/2024 06:21:34

Provedor de dados: | 19
País: | Japan
Título: | Neospora caninum: Application of apical membrane antigen 1 encapsulated in the oligomannose-coated liposomes for reduction of offspring mortality from infection in BALB/c mice
Autores: | Zhang, Houshuang; Nishikawa, Yoshifumi; Ikehara, Yuzuru; Kojima, Naoya; Yokoyama, Naoaki; Xuan, Xuenan.
Data: | 2010-06
Ano: | 2010
Palavras-chave: | Neospora caninum; Apical membrane antigen 1; Oligomannose-coated liposomes.
Resumo: | Liposomes coated with neoglycolipids constructed with mannopentaose and  dipalmitoylphosphatidylethanolamine (Man3-DPPE), referred to as M3-DPPE  liposomes, have been shown to induce cellular immunity against antigens encapsulated therein. To evaluate whether these M3-DPPE liposomes have an  adjuvant capacity against Neospora caninum infection, a novel immunization  method utilizing soluble N. caninum apical membrane antigen 1 (NcAMA1)  encapsulated in the M3-DPPE liposomes (M3-NcAMA1) was employed. The  intent was to reduce offspring mortality from N. caninum infection in susceptible,  pregnant BALB/c mice. The results revealed that BALB/c mice developed IgG  antibodies specific to N. caninum. A significant amount of interferon (IFN)-γ  production was detected in culture supernatants of NcAMA1 protein- or N.  caninum lysate-stimulated spleen cells obtained from the mice one week after the  third immunization with M3-NcAMA1. This suggested that the T helper-type 1  (Th1) immune response was induced in the mice. The parasite burden in the  dams’ brain tissue was decreased in M3-NcAMA1-immunized mice. Moreover,  the survival rate of offspring increased significantly in mice immunized with M3-  NcAMA1. Taken together, the results demonstrated that a parasite-specific Th1  immune response was successfully induced in the pregnant mice immunized with  M3-NcAMA1. Thus, an effective reduction of offspring mortality from N.  caninum infection was triggered.
Idioma: | Inglês
Identificador: | http://ir.obihiro.ac.jp/dspace/handle/10322/2821
Editor: | ELSEVIER
Formato: | application/pdf
Fonte: | Elsevier Inc.