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|Title:||Properdin plays a protective role in polymicrobial septic peritonitis|
|Authors:||Stover, Cordula M.|
Luckett, Jeni C.
Figgitt, Sue E.
Mannel, Daniela M.
Schwaeble, Wilhelm J.
|Publisher:||American Association of Immunologists|
|Citation:||Journal of Immunology, 2008, 180, pp. 3313-3318.|
|Abstract:||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.|
|Description:||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/.|
|Appears in Collections:||Published Articles, Dept. of Infection, Immunity and Inflammation|
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