Introduction Brucella is a Gram-negative facultative intracellular bacterium that can cause fever, abortion, and other symptoms in humans and various mammals. btpB , a type IV secretion system (T4SS) effector of Brucella , plays a critical role in regulating Brucella infection and inhibiting the host's innate immune response. Methods In this study, a btpB mutant strain of Brucella A19 (Δ btpB ) was constructed using homologous recombination, and its biological characteristics, virulence, and immunogenicity were systematically investigated. Results The results showed that Δ btpB exhibited weakened resistance to in vitro stress, while its growth characteristics did not differ significantly from the wild-type strain A19. In the mouse immunization model, Δ btpB induced weaker splenic pathological damage, and the splenic bacterial load was significantly lower than that of A19, indicating its reduced virulence. Additionally, Δ btpB infection elicited stronger humoral and cellular immune responses in mice, including higher antibody levels, increased levels of Th1 cytokines (such as IFN-γ and IL-2), and enhanced proliferation and activity of CD8+ cells. Detection of Th1 and Th2 cells revealed that Δ btpB induced stronger Th1 and Th2 responses in the spleen in the early stage, but the Th2 response weakened in the middle and late stages of infection. Notably, Δ btpB infection did not suppress natural killer (NK) cell activity and even significantly enhanced its cytotoxic activity compared to the A19 strain. Conclusion Our research demonstrates that Δ btpB leads to a reduced survival capacity of Brucella , while enhancing its immunogenicity. This suggests btpB is an important target for the prevention of Brucella .
Yu et al. (Fri,) studied this question.