Brucella abortus Omp19 recombinant protein subcutaneously co-delivered with an antigen enhances antigen-specific T helper 1 memory responses and induces protection against parasite challenge

• DOI: 10.1016/j.vaccine.2015.12.012
• Publication Date: 2015-12-18T08:17:04Z
• Authors: Lorena M. Coria; Andrés E. Ibañez; Karina A. Pasquevich; Paula L. González...; Fernanda M. Frank; Guillermo H. Giam...; Juliana Cassataro
• Keywords: 0301 basic medicine; Ovalbumin; T Helper 1; Lipoproteins; Brucella abortus; Antigens, Protozoan; Lymphocyte Activation; Mice; 03 medical and health sciences; Adjuvants, Immunologic; https://purl.org/becyt/ford/3.1; Animals; https://purl.org/becyt/ford/3; Adjuvant; Cells, Cultured; Antigens, Bacterial; Immunity, Cellular; Mice, Inbred BALB C; Dendritic Cells; Outer Membrane Protein; Brucella; Antibodies, Bacterial; Recombinant Proteins; 3. Good health; Mice, Inbred C57BL; Cattle; Female; Vaccine; Immunologic Memory; Bacterial Outer Membrane Proteins

The discovery of effective adjuvants for many vaccines especially those with limited commercial appeal, such as vaccines to poverty-related diseases, is required. In this work, we demonstrated that subcutaneous co-administration of mice with the outer membrane protein U-Omp19 from Brucella spp. plus OVA as antigen (Ag) increases Ag-specific T cell proliferation and T helper (Th) 1 immune responses in vitro and in vivo. U-Omp19 treated dendritic cells promote IFN-γ production by specific CD4(+) T cells and increases T cell proliferation. U-Omp19 co-administration induces the production of Ag specific effector memory T cell populations (CD4(+) CD44(high) CD62L(low) T cells). Finally, subcutaneous co-administration of U-Omp19 with Trypanosoma cruzi Ags confers protection against virulent parasite challenge, reducing parasitemia and weight loss while increasing mice survival. These results indicate that the bacterial protein U-Omp19 when delivered subcutaneously could be a suitable component of vaccine formulations against infectious diseases requiring Th1 immune responses.