Antibody-mediated bacterial clearance from the lower respiratory tract of mice requires complement component C3

Authors

  • Elizabeth J. Pishko,

    1. Department of Veterinary Science, The Pennsylvania State University, University Park, USA
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    • The first two authors contributed the majority of the writing (E.J.P.) and the experimentation (G.S.K.).

  • Girish S. Kirimanjeswara,

    1. Department of Veterinary Science, The Pennsylvania State University, University Park, USA
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  • Mylisa R. Pilione,

    1. Department of Veterinary Science, The Pennsylvania State University, University Park, USA
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  • Lakshmi Gopinathan,

    1. The Huck Institutes of Life Sciences, The Pennsylvania State University, University Park, USA
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  • Mary J. Kennett,

    1. Department of Veterinary Science, The Pennsylvania State University, University Park, USA
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  • Eric T. Harvill

    Corresponding author
    1. Department of Veterinary Science, The Pennsylvania State University, University Park, USA
    2. Department of Biochemistry, Microbiology and Molecular Biology, The Pennsylvania State University, University Park, USA
    3. The Huck Institutes of Life Sciences, The Pennsylvania State University, University Park, USA
    • The Pennsylvania State University, Department of Veterinary Science, 115 Henning Bldg., University Park, PA 16802, USA Fax: +1-814-863-6140
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Abstract

To assess the contribution of complement to respiratory immunity in the context of a natural bacterial infection, we used mice genetically deficient in complement components and the murine pathogen Bordetella bronchiseptica. Complement component C3 was not required for the control of bacterial infection or for the generation of infection-induced protective immunity. However, C3-deficient (C3–/–) mice were severely defective, compared to wild type, in vaccine-induced protective immunity. Adoptively transferred immune serum from convalescent wild-type or C3–/– animals rapidly cleared B. bronchiseptica from the lungs of wild-type mice but did not affect its growth in C3–/– mice, indicating that the defect is not in the generation of protective immunity, but in its function. Immune serum was effective in C5-deficient mice but had little effect in the lungs of mice lacking either Fcγ receptors (FcγR) or CR3, suggesting bacterial clearance is not via direct complement-mediated lysis. Together, these data indicate that complement is required for antibody-mediated clearance of Bordetella and suggest the mechanism involves C3 opsonization of bacteria for phagocytosis that is both CR3- and FcγR-dependent.

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