Submitted to: Infection and Immunity
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 4/30/1995
Publication Date: N/A
Interpretive Summary: Cattle are currently given the Brucella abortus strain 19 vaccine to prevent brucellosis and abortions that are caused by the bacteria, B. abortus. The B. abortus strain RB51 vaccine is being tested to replace the strain 19 vaccine for use in cattle. Strain RB51 is better than strain 19 as a vaccine because cattle vaccinated with RB51 can be easily tested to determine if they have brucellosis. In testing the RB51 vaccine, it is important to determine if strain RB51 and 19 stimulate immune responses to the same parts, called antigens, that are present in B. abortus that infects cattle. Results from this study indicated that vaccination of mice with strain RB51 or 19 stimulates immune responses to the same protein antigens of B. abortus and these responses result in protective immunity from infection with B. abortus. The results also indicated that protective immunity in mice vaccinated with strain 19, but not with strain RB51, may have arisen from certain types of immune responses to another antigen of B. abortus, called lipopolysaccharide. The findings suggest that immune responses to proteins but not to lipopolysaccharide are important in providing protective immunity from brucellosis in mice and perhaps also in cattle that have been vaccinated with strain RB51.
Technical Abstract: Mice vaccinated with Brucella abortus 19 (S19) or with the lipopolysaccharide (LPS) O-antigen-deficient mutant, strain RB51 (SRB51), had spleen cells following vaccination and following challenge infection with B. abortus 2308 (S2308) which proliferated in response to 32, 27, 18, and >18 kDa proteins, but not to 106, 80, and 49 kDa proteins of S2308. Spleen cells obtained from SRB51- vaccinated mice following vaccination or challenge infection with S2308 and cells from S19-vaccinated mice following vaccination did not have increased proliferation in response to S2308 LPS. However, spleen cells from S19-vaccinated mice following challenge infection with S2308 did have increased proliferation to S2308 LPS. We previously reported that mice vaccinated with S19 or SRB51 which were analyzed in the current study have increased resistance to infection with S2308 and that only mice vaccinated with S19 produce antibody to S2308 LPS (Infect. Immun. 63:264-270, 1995). Results from our current and previous study support the contention that vaccination of mice with S19 or SRB51 induced protection from infection with S2308 by cell-mediated immune responses to the same immunodominant protein antigens of S2308. In addition, LPS-responsive spleen cells and antibody to S2308 LPS may contribute to protective immunity in mice vaccinated with S19 but not in mice vaccinated with SRB51.