Figure 1.
Overview of antibody-mediated protection against A. baumannii. Virulent strains appear to be resistant to direct bactericidal activity via membrane attack complex formation. A. baumannii-specific antibodies, however, still mark the pathogen for C3b deposition on its surface by activation of the classical complement pathway. C3a is released to increase phagocyte recruitment to the site of infection. In the absence of complement, antibodies continue to identify the bacterium for increased phagocytosis through antibody-Fc receptor interactions. Additionally, antibodies generated toward virulence factors required for pathogenesis, such as siderophores, can attenuate A. baumannii’s virulence.