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CUTTING EDGE |
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Department of Molecular Biology, Max Planck Institute for Infection Biology, Berlin, Germany;
Department of Infection Biology, Max Planck Institute for Biology, Tubingen, Germany; and
Department of Molecular Microbiology, Biozentrum of the University of Basel, Basel, Switzerland
The genus Bartonella includes important human-specific and zoonotic pathogens which cause intraerythrocytic bacteremia in their mammalian reservoir host(s). It is accepted that cellular immunity plays a decisive role in the host’s defense against most intracellular bacteria. Bartonella sp. infection in the immunocompetent host typically leads to immunity against homologous challenge. The basis of this immunity, be it cellular or humoral, is unclear. In this study, the course of Bartonella grahamii bacteremia in immunocompetent and immunocompromised mice was compared. In immunocompetent hosts, the bacteremia is transient and induces a strong humoral immune response. In contrast, bacteremia persists in immunocompromised B and T cell-deficient mice. Immune serum transfer beginning with day 6 postinfection to B cell-deficient mice unable to produce Igs converted the persistent bacteremia to a transient course indistinguishable from that of immunocompetent animals. These data demonstrate an essential role for specific Abs in abrogating the intraerythrocytic bacteremia of B. grahamii in mice.
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