Intranasal administration of chlamydial outer protein N (CopN) induces protection against pulmonary Chlamydia pneumoniae infection in a mouse model

被引:17
|
作者
Tammiruusu, A.
Penttila, T.
Lahesmaa, R.
Sarvas, M.
Puolakkainen, M.
Vuola, J. M.
机构
[1] Natl Publ Hlth Inst, Infect Pathogenesis Lab, Dept Viral Dis & Immunol, FIN-00300 Helsinki, Finland
[2] Univ Helsinki, HUSLAB, Diagnost Lab, Haartman Inst,Dept Virol, FIN-00014 Helsinki, Finland
[3] Turku Univ, Turku Ctr Biotechnol, FIN-20520 Turku, Finland
[4] Abo Akad Univ, FIN-20520 Turku, Finland
[5] Natl Publ Hlth Inst, Dept Vaccines, FIN-00300 Helsinki, Finland
基金
芬兰科学院;
关键词
Chlamydia pneunoniae; CopN; immunization;
D O I
10.1016/j.vaccine.2006.07.043
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Chlamydia pneunioniae is an intracellular pathogen that grows inside a vacuole, referred to as an inclusion. C. pnetanoniae possess a type III secretion system (TTSS), which allows them to secrete effector molecules into the inclusion membrane and to the host cell cytosol. Proteins such as chlamyclial outer protein N (CopN) that associate with the inclusion membrane are potential targets for the host's MHC-dependent antigen presentation. thereby representing ideal antigen candidates for T cell-based vaccination. The results of this study showed that intranasal immunization of BALB/c mice with heat-aggregated CopN protein and an Escherichia coli heat-labile toxin (LT) induced a strong immune response. detected as antigen-specific antibody production, lymphocyte proliferation and IFN-gamma production. Furthermore, the immunization induced statistically significant protection against intranasal C. pneunioniae challenge, the level of which correlated with the magnitude of CopN-specific lymphocyte proliferation. Both heat-aggregation of the antigen and the presence of LT adjuvant were required for maximal protective effect. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:283 / 290
页数:8
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