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Properdin plays a protective role in polymicrobial septic peritonitis

By Cordula M. Stover, Jeni C. Luckett, Bernd Echtenacher, Aline Dupont, Sue E. Figgitt, Jane Brown, Daniela M. Mannel and Wilhelm J. Schwaeble

Abstract

This article was published as Journal of Immunology, 2008, 180, pp. 3313-3318. Copyright © American Association of Immunologists. It is available from http://www.jimmunol.org/.Properdin 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 DH5α. 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 DH5α. We conclude that properdin plays a significant role in the outcome of polymicrobial sepsis

Publisher: American Association of Immunologists
Year: 2008
OAI identifier: oai:lra.le.ac.uk:2381/4032
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