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Properdin Deficiency in Murine Models of Nonseptic Shock¹

Nina D. Ivanovska^2,*, Petya A. Dimitrova^2,*, Jeni C. Luckett, Rana El-Rachkidy Lonnen, Wilhelm J. Schwaeble and Cordula M. Stover^3,

^* Department of Immunology, Institute of Microbiology, Bulgarian Academy of Sciences, Sofia, Bulgaria; and Department of Infection, Immunity and Inflammation, University of Leicester, Leicester, United Kingdom

Hereditary properdin deficiency is linked to susceptibility to meningococcal disease (Neisseria meningitidis serotypes Y and W-135) with high mortality. Its relative contribution toward the outcome of nonseptic shock has not been investigated. Using properdin-deficient C57BL/6 mice and their littermates, this study examines their survival of zymosan-induced and LPS-induced shock. Properdin-deficient mice were more resistant to zymosan shock compared with wild-type mice, which showed greater impairment of end-organ function 24 h after zymosan injection, higher TNF- production by alveolar and peritoneal macrophages, higher TNF-, and, inversely, lower IL-10 levels in peritoneal lavage and circulation and higher plasma C5a levels. Properdin-deficient mice showed significantly higher mortality in LPS shock, elevated TNF-, and, inversely, reduced IL-10 production by peritoneal macrophages as well as lower plasma C5a levels compared with wild-type littermates. NO production by peritoneal macrophages and plasma 1-antitrypsin levels at 24 h after the injection of LPS or zymosan were decreased in properdin-deficient mice in both models, and fewer histopathologic changes in liver were observed in properdin-deficient animals. This study provides evidence that properdin deficiency attenuates zymosan-induced shock and exacerbates LPS-induced shock.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This study was supported by Medical Research Council Grant G0400300 (to C.M.S.).

² N.D.I. and P.A.D. contributed equally to this work.

³ Address correspondence and reprint requests to Dr. Cordula Stover, Lecturer in Immunology, Department of Infection, Immunity and Inflammation, University of Leicester, University Road, Leicester LE1 9HN, U.K. E-mail address: cms13{at}leicester.ac.uk

⁴ Abbreviations used in this paper: WT, wild type; aM, alveolar macrophage; pM, peritoneal macrophage.

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