• Cordula M Stover, Jeni C Luckett, Bernd Echtenacher, Aline Dupont, Sue E Figgitt, Jane Brown, Daniela N Männel, and Wilhelm J Schwaeble.
• Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, UK. cms13@le.ac.uk
• J. Immunol. 2008 Mar 1; 180 (5): 3313-8.

AbstractProperdin is a positive regulator of complement activation so far known to be instrumental in the survival of infections with certain serotypes of Neisseria meningitidis. We have generated a fully backcrossed properdin-deficient mouse line by conventional gene-specific targeting. In vitro, properdin-deficient serum is impaired in alternative pathway-dependent generation of complement fragment C3b when activated by Escherichia coli DH5alpha. Properdin-deficient mice and wild-type littermates compare in their levels of C3 and IgM. In an in vivo model of polymicrobial septic peritonitis induced by sublethal cecal ligation and puncture, properdin-deficient mice appear immunocompromised, because they are significantly impaired in their survival compared with wild-type littermates. We further show that properdin localizes to mast cells and that properdin has the ability to directly associate with E. coli DH5alpha. We conclude that properdin plays a significant role in the outcome of polymicrobial sepsis.

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