Background & Objectives: Lipopolysaccharide (LPS) is the main antigenic structure expressed on the surface of smooth strains of Brucella. It has been shown that Outer membrane vesicle (OMV) of Neisseria meningitidis efficiently promote IgG and IgM response against the administrated antigen as an adjuvant. The aim of this study is to evaluate the effect of LPS-OMV noncovalent complex in producing of T helper 1 cytokine (IFN-γ) and T helper 2 cytokines (IL-4 and IL-10) in mice.

  Methods: LPS extracted by an optimized method based on hot phenol-water extraction. Groups of six BALB/c mice were injected subcutaneously with LPS alone, LPS with Freund adjuvant and LPS-OMV complex on 0, 14 and 28 days. Levels of IFN-γ, IL-4 and IL-10 were evaluated in spleen cell suspension supernatant by ELISA.

  Result: Immunization with B. abortus LPS significantly induced high level of IFN-γ in comparison to the other groups immunized with LPS-OMV and LPS+ adjuvant (p<0.05). In contrast, lower levels of IL-4 and IL-10 were elicited by LPS in the rest groups. Immunization with the non-covalent complex of B. abortus LPS-N. meningitidis serogroup B OMV caused a significant increase of IL-4 and IL-10 compared with the mice immunized with B. abortus LPS (p<0.05), while the titer of IFN-γ is still significantly higher than IL-4 and IL-10 (p<0.05).

  Conclusion: The raise of IFN-γ following the immunization with all of the compounds (LPS, LPS-OMV non-covalent complex and LPS+adjuvant) indicates the activation of Th₁ population that would be correlated to the clearance of the organism due to the amplification of anti-microbial activity of Polymorphonuclear cells. Low levels of IL-4 and IL-10 following the immunization with all compounds would be a sign of Th₁ responses dominancy or inhibition of Th₂ population proliferation and activity. Such a cytokine pattern would be a sign of the efficiency of brucellosis subunit vaccine because Th₂ responses basically have no role in the immune responses against Brucella and may lead to the persistence of intracellular infection.