Mechanism study of recombinant Mycobacteria smegmatis pharmacon in the immunization against Helicobacter pylori

Objective: To study the immune mechanism of the recombinant Mycobacteria smegmatis (rMs) pharmacon aganist Helicobacter pylori (Hp) in BLAB/c mice. Methods: Seventy-five female BLAB/c mice were randomly divided into 5 groups, 4 weeks post-immunization and 4 weeks post-challenge. All mice were sacrificed, the blood, gastric and spleen tissue were collected. The cytokine expression of gastric and spleen was analyzed with semiquantitative reverse transcription-PCR. The levels of the Hp specific serum IgG, IgA, IgG1 and IgG2a was detected by ELISA. Multiplication of mouse lymphocytes was detected by MTT, and IgA of gastric tissue was investigated with immunohistochemistry. Results: The specific mucosal IgA and specific serum IgG were induced with the administration of rMs, and significant proliferation of spleen lymphocyte was observed in rMs group after the stimulation of Hp antigens. Meanwhile, rich IgA was found in the epithelium and lamina propria of immunized mice with rMs pharmacon as compared with PBS and Ms group mice after 4 weeks challenge. RT-PCR of cytokine revealed that every immunity group had relatively high levels of mRNA for IFN-γ, IL-12 and IL-2 but not IL-4, IL-6 and IL-10. After Hp attacked, the levels of IFN-γ, IL-12 and IL-2 mRNA expression of rMs groups were significantly lower than that of the PBS and Ms group (P < 0.05). While the level of IL-4 mRNA expression of rMs groups were significantly higher than that of the PBS and Ms group (P < 0.05). There was no significant difference among any rMs group (P > 0.05). Conclusion: TH1 and TH2 protective response can be elicited with rMs immunization.