engleski

Kinetics of Protective Cytokine, Antibody, and Cellular Immune Response to the B. Pertussis Infection in Mouse Model

The murine model of Bordetella pertussis respiratory infection was used to analyze mechanisms of protective immunity. Five weeks after infection normal adult BALB/c and C57BL/6 mice clear bacteria from respiratory tissue. The presence of CD4+ T cells specific for B. pertussis could be detected in regional lymph nodes of infected animals. The production of IFN-g, but not IL-4 nor IL-10 can be demonstrated in the supernatant of ex vivo stimulated T cells. Following the elimination of bacteria detectable titer of specific antibodies against B. pertussis appeared in serum andbronchoalveolar lavage fluid. Unlike this, the expression of inflammatory cytokines mRNA in lung tissue after infection correlates with the amount of B. pertussis bacteria cultured from respiratory tissue. Mice lacking in T and B cells (SCID), as well as those lacking only T cells (nude) die 3-5 weeks after infection. The immunodeficient mice show enhanced expression of inflammatory cytokines mRNA (IFN-g, IL-6, IL-12, TNF-a) at the death time. The expression of IFN-g mRNA in lung of normal mice appear a week after the infection and then subsequently declined. In vivo neutralization of IFN g by antibodies abrogated protective immunity. Similarly, IFN g knockout mice were sensitive to infection. Unlike that, IL-4 neutralization does not affect the number of cultured bacteria from the infected tissue. These results indicate that early phase IFN-g activity and cells specific immunity play the critical role in controlling B. pertussis infection. Interestingly measurable titers of antibodies come much later, in the resolution phase of infection.

immune response; cytokine; antibody; B. pertussis; protection

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